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- ArticleAçık Erişim2023The effects of metyrosine on ischemia-reperfusion-induced oxidative ovarian injury in rats: Biochemical and histopathological assessment
Yapca, Omer E.; Yildiz, Gulsah A.; Mammadov, Renad; Kurt, Nezahat; Gundogdu, Betul; Arslan, Yusuf K.; Suleyman, Halis; Cetin, Nihal
The aim of this study is to investigate the effect of metyrosine on ischemia-reperfusion (I/R) induced ovarian injury in rats in terms of biochemistry and histopathology. Rats were divided into: ovarian I/R (OIR), ovarian I/R+50 mg/kg metyrosine (OIRM) and sham (SG) operations. OIRM group received 50 mg/kg metyrosine one hour before the application of the anesthetic agent, OIR and SG group rats received equal amount of distilled water to be used as a solvent orally through cannula. Following the application of the anesthetic agent, ovaries of OIRM and OIR group rats were subjected to ischemia and reperfusion, each of which took two hours. This biochemical experiment findings revealed high levels of malondialdehyde (MDA) and cyclo-oxygenase-2 (COX-2) and low levels of total glutathione (tGSH), superoxide dismutase (SOD) and cyclo-oxygenase-1 (COX-1) in the ovarian tissue of OIR group, with significant histopathological injury. In metyrosine group, MDA and COX-2 levels were lower than the OIR group whereas tGSH, SOD and COX-1 levels were higher, with slighter histopathological injury. Our experimental findings indicate that metyrosine inhibits oxidative and pro-inflammatory damage associated with ovarian I/R in rats. These findings suggest that metyrosine could be useful in the treatment of ovarian injury associated with I/R.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023Effect of anakinra, tocilizumab, and the combination thereof on bladder ischemia-reperfusion damage in albino Wistar-type rats; [Efecto de la anakinra, el tocilizumab y la combinación de ambos sobre el daño por isquemia-reperfusión vesical en ratas albinas tipo Wistar]
Bicer, Senol; Suleyman, Bahadir; Mammadov, Renad; Yavuzer, Bulent; Cicek, Betul; Altuner, Durdu; Coban, Taha A.; Suleyman, Halis
Several studies have reported that oxidative stress, and proinflam-matory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-one beta (IL-1β), and interleukin-six (IL-6) are the main factors underlying bladder ischemia-reperfusion (I/R) damage. Anakinra and tocilizumab are known to be antioxidants and proinflammatory cytokine inhibitors. Our study aims to investigate if anakinra, tocilizumab, and the combination (ATC) thereof have a protective effect against oxidative and inflammatory bladder damage induced through the I/R procedure in rats, and evaluate by comparing these compounds. Male rats were divided into five groups: bladder sham-operation applied group (SG); bladder only I/R applied group (IRG); anakinra+bladder I/R applied group (AIR); tocilizumab+bladder I/R applied group (TIR); and ATC+bladder I/R applied group (ATIR). An atraumatic clamp was placed on the abdominal aorta of animals in all groups (except SG), and one hour of ischemia followed by two hours of reperfusion was performed. Our biochemical find-ings showed that anakinra and tocilizumab significantly inhibited the increase of oxidant malondialdehyde (MDA) and the decrease of antioxidants such as total glu-tathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) in bladder tissue by I/R, both at the same levels. Furthermore, anakinra and tocilizumab significantly suppressed the I/R-associated increase of TNF-α, IL-1β, and IL-6 in bladder tissue. ATC was the one that best prevented the I/R-related increase in MDA, TNF-α, IL-1β, and IL-6 and the decrease in tGSH, SOD, and CAT in the bladder tissue. ATC was more beneficial than anakinra or tocilizumab alone in treating bladder I/R damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effects of benidipine, paracetamol, and their combination on postoperative and normal tissue pain thresholds
Bedir, Zehra; Ozkaloglu Erdem, Kezban Tuna; Doymus, Omer; Suleyman, Halis; Yavuzer, Bulent; Cicek, Betul; Altuner, Durdu; Mammadov, Renad; Yilmaz, Mehmet; Coban, Taha Abdulkadir
Introduction: In clinical practice, inadequate pain inhibition leads to increased morbidity and mortality. Increased intracellular calcium, oxidants, and proinflammatory cytokines are known to play a role in the pathogenesis of postoperative pain. Therefore, we investigated the analgesic effects of benidipine, paracetamol, and benidipine-paracetamol combination (BPC) on postoperative and normal pain thresholds in rats. Material and methods: Sixty-four male albino Wistar rats weighing 285–295 g were used. The without-incision rats were divided into 4 subgroups: healthy control, benidipine alone, paracetamol alone, and BPC. The scalpel-incision rats were divided into 4 subgroups: scalpel incision, scalpel incision + benidipine, scalpel incision + paracetamol, and scalpel incision + BPC. Paw pain thresholds of rats were measured using a Basile algesimeter. Biochemical analyses were performed on the paw tissues of 6 rats randomly taken from the experimental groups, each containing 8 rats. Rats were sacrificed immediately after the measurements. After the pain threshold tests were finished, the paw tissues were removed and malondialdehyde (MDA), total glutathione (tGSH), cyclooxygenase (COX), and interleukin-6 (IL-6) levels were measured. Results: There was no significant difference between the groups in paw pain threshold and measured biochemical parameters in rats without incision. The decrease in the pain threshold of the incised paw was also best prevented by BPC, followed by benidipine and then paracetamol. Furthermore, increases in scalpel-incised paw tissue MDA, COX-2, and IL-6 levels and the decrease in tGSH were significantly suppressed by benidipine and BPC, while paracetamol could only significantly inhibit the increase in IL-6 production. Conclusion: The combination of the L-type Ca2+ channel blocker benidipine and paracetamol (BPC) may provide potent analgesia. Our experimental results support that BPC may be useful in the treatment of severe pain that cannot be adequately inhibited by paracetamol.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023The role of Hippophae rhamnoides L. on 5-fluorouracil-ınduced oral mucositis in rats
Dilber, Muhammet; Suleyman, Bahadir; Mammadov, Renad; Suleyman, Zeynep; Yavuzer, Bulent; Gulaboglu, Mine; Erhan, Ertugrul; Salcan, Ismail; Suleyman, Halis
Current study aimed to research the effect of Hippophae rhamnoides (HRE) on potantial oral oxidative and inflammatory damage of 5-FU in rats. The rats were assigned to three groups; healthy (HG), 5-FU 100mg/kg (FUG) and HRE 50mg/kg +5-FU 100mg/kg (HRFU). The 5-FU was injected in the FUG group intraperitoneally. The HRFU was injected 5-FU at 100mg/kg IP one hour after the 50mg/kg HRE was given orally. Olive oil was used as a solvent for the HG. HRE was given to the rats three times a day for ten days. 5-FU was given one dose on the 1st, 3rd and 5th days. On the 10th day, the tissues removed from the animals were euthanized with high-dose anaesthesia and were macroscopically examined. The levels of the oxidant, antioxidant and proinflammatory cytokines were investigated.It was seen that HRE alleviated the symptoms of severe mucositis by antagonizing the effects of 5-FU on oxidant, antioxidant and proinflammatory cytokines such as malondialdehyde, total glutathione, superoxide dismutase, catalase, nuclear factor kappa-B and interleukin-6 in inner cheek and tongue tissue. These results recommend that HRE may be benefical in the cure of 5-FU-associated oral mucositis.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effect of Usnea longissima ethyl acetate extract on acute oxidative and inflammatory lung damage from Staphylococcus aureus infection in rats
Dabanlioglu, Bulent; Suleyman, Bahadir; Mammadov, Renad; Yavuzer, Bulent; Akyuz, Sumeyye; Akkas, Onder; Mokhtare, Behzad; Turumtay, Emine Akyuz; Altuner, Durdu; Coban, Taha Abdulkadir
The role of oxidants and proinflammatory cytokines in the pathogenesis of pneumonia caused by Staphylococcus aureus (S. aureus) has been demonstrated. The present study aims to investigate the protective effect of ethyl acetate extract (EtOAc) obtained from Usnea longissima (UL) against acute oxidative and inflammatory lung damage due to S. aureus infection in rats. Albino Wistar-type male rats were divided into three groups: Healthy (HG), S. aureus inoculated (SaG), and S. aureus inoculated + ULEtOAc administered (SUL). SaG (n = 6) and SUL (n = 6) group rats’ left nostrils (excluding HG) were inoculated with 0.1 ml bacterial mixture. After 24 hours, ULEtOAc (50 mg/kg) was administered orally to the SUL group, and the same volume of normal saline was administered orally to the HG (n = 6) and SaG groups. This procedure was performed once a day for seven days. Levels of oxidant and antioxidant parameters such as malondialdehyde (MDA) and total glutathione (tGSH), as well as pro-inflammatory cytokine levels such as nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-one beta (IL-1β), were measured in removed lung tissues. Tissues were also examined histopathologically. Biochemical results showed that ULEtOAc significantly suppressed the increase of MDA, NF-κB, TNF-α, and IL-1β levels and the decrease of tGSH caused by S. aureus in lung tissue. S. aureus inoculation caused severe mononuclear cell infiltration in interstitial areas, severe lymphoid hyperplasia in bronchial-associated lymphoid tissue and severe alveolar edema, histopathologically. Treatment with ULEtOAc had an attenuating effect on these histopathological findings. Experimental results from this study suggest that ULEtOAc may be beneficial in treating S. aureus-induced oxidative and inflammatory lung damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effect of felodipine on indomethacin-induced gastric ulcers in rats
Akbaş, Nergis; Süleyman, Bahadır; Mammadov, Renad; Gülaboğlu, Mine; Akbaş, Emin Murat; Süleyman, Halis
Felodipine is a calcium channel blocker with antioxidant and anti-inflammatory properties. Researchers have stated that oxidative stress and inflammation also play a role in the pathophysiology of gastric ulcers caused by nonsteroidal anti-inflammatory drugs. The aim of this study was to investigate the antiulcer effect of felodipine on indomethacin-induced gastric ulcers in Wistar rats and compare it with that of famotidine. The antiulcer activities of felodipine (5 mg/kg) and famotidine were investigated biochemically and macroscopically in animals treated with felodipine (5 mg/kg) and famotidine in combination with indomethacin. The results were compared with those of the healthy control group and the group administered indomethacin alone. It was observed that felodipine suppressed the indomethacin-induced malondialdehyde increase (P<0.001); reduced the decrease in total glutathione amount (P<0.001), reduced the decrease superoxide dismutase (P<0.001), and catalase activities (P<0.001); and significantly inhibited ulcers (P<0.001) at the tested dose compared with indomethacin alone. Felodipine at a dose of 5 mg/kg reduced the indomethacin-induced decrease in cyclooxygenase-1 activity (P<0.001) but did not cause a significant reduction in the decrease in cyclooxygenase-2 activity. The antiulcer efficacy of felodipine was demonstrated in this experimental model. These data suggest that felodipine may be useful in the treatment of nonsteroidal anti-inflammatory drug-induced gastric injury.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023Protective Effect of Adenosine Triphosphate Against Bevacizumab-Induced Mandibular Bone Damage in Rats
Yalcin, Ertan; Bayramoglu, Zeynep; Mammadov, Renad; Altuner, Durdu; Bulut, Seval; Yavuzer, Bulent; Mokhtare, Behzad; Coban, Taha Abdulkadir; Suleyman, Halis; Suleyman, Bahadir
Bevacizumab is the anticancer drug used as an anti-angiogenic inhibitor of vascular endothelial growth factor (VEGF)-A. Bevacizumab causes toxicity by decreasing adenosine triphosphate (ATP) and increasing through reactive oxygen species (ROS) production. Male Albino Wistar rats were divided into 3 groups healthy (HG), bevacizumab administered (BVZ) and ATP+bevacizumab administered (ATP+BVZ). In the ATP+BVZ group, 25mg/kg ATP was injected between the mandibular gingiva and the bone. One hour after the application, 10 mg/kg bevacizumab was administrated intraperitoneally to the ATP+BVZ and BVZ groups. Two doses of bevacizumab were administered on the 1st and 15th days. ATP administration was continued once a day for 30 days. intoATP significantly prevented the increase in malondialdehyde (MDA) and total oxidant status (TOS) levels and the decrease in total glutathione (tGSH) and total antioxidant status (TAS) levels in the mandible bone tissue. ATP alleviated the histopathological damage associated with bevacizumab.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023The preventive effect of exogenous adenosine triphosphate on methanol-induced cardiotoxicity in rats
Coskun, Resit; Celik, Aziz Inan; Cosgun, Muharrem Said; Mammadov, Renad
Exposure to methanol can cause serious consequences such as permanent visual disturbances and death. The heart tissue is highly vulnerable to ATP deficiency. Our study aimed to investigate whether exogenous ATP administration may alleviate methanol-induced ATP deficiency and subsequent oxidative damage in rat heart tissue. A total of 30 rats were divided into equal five groups; Healthy Group (HG), Methotrexate (MXG), Methanol (MeOH), Methotrexate+Methanol (MXM), and Methotrexate+Methanol+ATP (MMA) groups. We inhibited tetrahydrofolate synthesis by methotrexate to induce methanol toxicity. Methotrexate was administered to MXG, MXM, and MMA group animals for seven days with a catheter directly to the stomach at a 0,3 mg/kg dose per day. At the end of this period, % 20 methanol at a dose of 3 g/kg was administered to MeOH, MMA and MXM group animals. Immediately after methanol application, MMA group animals were injected with ATP at a 4 mg/kg dose intraperitoneally. Blood samples and heart tissues were used for biochemical analysis and histopathological examination. Co-exposure to methanol and methotrexate substantially exacerbated cardiac damage, indicating the potent cardiotoxic effects of methanol. However, the administration of exogenous ATP to MMA group animals brought biochemical oxidative damage parameters and histopathological findings closer to HG.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Tocilizumab is effective in preventing ovarian injury induced by ischemia-reperfusion in rats
Uzel, Kemine; Lakhno, Igor; Turkler, Can; Kuzucu, Mehmet; Yazici, Gulce Naz; Mammadov, Renad; Suleyman, Bahadir; Kale, Ahmet; Suleyman, Halis
Ovarian torsion can be defined as the bending of the ovaries on the supporting ligament, disrupting both venous and arterial blood circulation. Insufficient blood flow causes ovarian tissue hypoxia and leads to ischemia. This study aimed to investigate whether tocilizumab has a protective effect on ischemia-reperfusion injury due to ovarian torsion in rats. Eighteen female Wistar albino rats were divided into three equal groups (Sham (SG), ischemia-reperfusion (OIR), and ischemia-reperfusion+tocilizumab (OIRT)). Degeneration, necrosis, vascular dilatation/congestion, interstitial edema, hemorrhage, and polymorphonuclear lymphocyte (PMNL) infiltration scores were significantly different between the groups (p=0.001 for all parameters). Moreover, the OIRT group had a significant improvement in these criteria compared to the OIR group (p<0.05). Additionally, there was a considerable difference between OIRT and OIR groups in the number of primordial, developing, and atretic follicles groups (p<0.05), while there was no difference in the number of corpus luteum (p=0.052). Stress markers or cytokines, such as MDA, tGSH, NF-κB, TNF-α, IL-1β, and IL-6, were significantly different between groups (p<0.05). Furthermore, a significant improvement was found in the measured variables when the OIRT group was compared with the OIR group (p<0.05). Tocilizumab may be an alternative option for treating ischemia-reperfusion injury due to ovarian torsion.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023Protective Effect of Lycopene against Ethanol-induced Oxidative Kidney Damage in Rats
Yilmaz, Canan Tuz; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Gursul, Cebrail; Yazici, Gulce Naz; Gulaboglu, Mine; Suleyman, Halis
SUMMARY. Alcohol consumption can have dramatic effects on organs and tissue cells, with kidneys being some of the most affected organs. This study investigates the effect of lycopene on ethanol-induced oxidative kidney damage in rats. Albino Wistar rats were randomly divided into three groups. The first group served as the healthy group (HG), receiving distilled water as a solvent; the second group was the ethanol group (EtON), receiving only ethanol; the third group received both lycopene and ethanol (LEt). While ethanol ad-ministration increased malondialdehyde (MDA), total oxidant status (TOS), and oxidative stress index (OSI) levels, it caused a decrease in total glutathione (tGSH) and total antioxidant status (TAS) levels. Also, ethanol caused histopathological damage to the kidney. It has been observed that lycopene inhibits ethanol-induced biochemical and histopathological changes in kidney tissue. Lycopene inhibited the change in the oxidant-anti-oxidant balance towards oxidants under ethanol treatment and prevented ethanol-associated kidney oxidative damage.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023Effect of Ketorolac and Nimesulide Combination on Surgical Pain, Stomach and Kidneys
Isik, Bahar; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Yavuzer, Bulent; Altuner, Durdu; Gulaboglu, Mine; Suleyman, Halis
Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID). Cyclooxygenase-2 (COX-2) inhibition from the therapeutic effects of NSAIDs and COX-1 inhibition from toxic effects are held responsible. It is known that nimesulide has formed a protective effect by inhibiting the decrease in COX-1 activity and the increase in COX-2 activity. In this study animals were divided into healthy (HG), paw-scalpel incision (PSI) control (PSIC), PSI+nimesulide (PSIN), PSI+ketorolac (PSIK), and PSI+nimesulide+ketorolac (PSI+NKC) administered groups. Nimesulide was administered orally(50 mg/kg), and ketorolac was administered intra-peritoneally(5 mg/kg). Nimesulide and ketorolac showed similar analgesia (p = 0.194), while NKC provided the best analgesia (p < 0.001). Nimesulide inhibited the increase of oxidant and COX-2 in gastric tissue and increased antioxidant and COX-1 levels, protecting the stomach tissue from ketorolac damage(p < 0.01). In addition, NKC reduced the area and number of ketorolac-induced gastric ulcers in the stomach (p<0.001). Nimesulide also prevented ketorolac-induced renal dysfunction (p < 0.001).
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023The Effect of Carvacrol on Oxidative and Inflammatory Liver Damage due to Staphylococcus aureus Infection in Rats
Dabanlioglu, Bulent; Suleyman, Bahadir; Mammadov, Renad; Coban, Taha Abdulkadir; Yazici, Gulce Naz; Akyuz, Sumeyye; Yavuzer, Bulent; Bulut, Seval; Suleyman, Halis
SUMMARY. Staphylococcus aureus is a bacterial pathogen that can cause oxidative stress. Carvacrol has anti-microbial, antioxidant, anti-inflammatory and hepatoprotective effects. This study evaluated the antibacterial effect of carvacrol and its effect on liver damage by S. aureus. The rats were divided into four groups: con-trol(HG), S. aureus injected (SaG), S. aureus + carvacrol (SaC), and S. aureus + cefazolin (SaCF). S. aureus was injected intraperitoneally (ip) to the SaG, SaC and SaCF groups. 24 h after the injection, carvacrol was given to the SaC group and cefazolin to the SaCF group as ip. Carvacrol and cefazolin administration was continued for 7 days. According to our antibiogram results, although the antibacterial effect of carvacrol was weaker than cefazolin, it prevented the increase of malondialdehyde (MDA), aminotransferase (ALT), aspar-tate aminotransferase (AST) and proinflammatory cytokines and the decrease of total glutathione (tGSH) better (p < 0.001). It also managed histopathological damage better than cefazolin. The results indicate that carvacrol may be helpful in the treatment of liver damage from infection.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023The Effect of Carvacrol on 5-Fluorouracil-Induced Optic Neuropathy in Rats. Histopathological and Biochemical Analysis
Cicek, Ibrahim; Altuner, Durdu; Suleyman, Zeynep; Mammadov, Renad; Coban, Taha Abdulkadir; Gulaboglu, Mine; Yazici, Gulce Naz; Bayrakceken, Kemal; Suleyman, Halis
5-Fluorouracil (5-FU) is also known to cause ocular toxicity. The purpose of this study was to investigate the effects of Carvacrol upon possible 5-FU-induced optic nerve damage in rats biochemically and histopathologically. In this study totally, eighteen albino Wistar male rats were used. The rats were grouped under three categories as the healthy (HG) (n=6), 100 mg/kg 5-FU treated alone (FUG) (n=6) and 50 mg/ kg Carvacrol+100 mg/kg 5-FU (CFU) groups (n=6). Carvacrol at 50 mg/kg was injected intraperitoneally (ip) to the CFU group. The same volume of 0.9% NaCl was administered as the solvent ip to HG and FUG groups. One hour after administrating Carvacrol and solvent, 100 mg/kg 5-FU was ip injected to CFU and FUG groups. Carvacrol was administered once daily for 10 days. Three-dose 5-FU was administered on the 1st, 3rd, and 5th days as one dose each. On the 10th day, the animals were euthanised with high-dose anesthesia and optic nerve tissues were removed. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and Interleukin (IL-6) levels were measured in optic nerve tissues. The tissues were also examined histopathologically. The results obtained from HG and CFU groups were compared with the FUG group. Significantly higher MDA and IL-6 levels (p < 0.001) and significantly lower (p < 0.001) tGSH, SOD, and CAT levels were determined in optic nerve samples of the FUG group rather than HG and CFU groups. In histopathological analyses, determined that astrocyte and oligodendrocyte nuclei were mostly darkly stained, the majority of astrocytes were hypertrophied and degenerated, and some oligodendrocytes were degenerated in the FUG group unlike HG and CFU groups. Moreover, the optic nerve tissue was determined to be vacuolized and intensely edematous, and blood capillaries were intensely dilated and congested. In conclusion, 5-FU caused optic neuropathy due to oxidative and inflammatory damage, and Carvacrol reduced this oxidative and inflammatory damage and histopathological changes in tissues. This revealed that Carvacrol was possibly to be efficient upon 5-FU-induced optic nerve toxicity.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023ANTI-INFLAMMATORY, ANALGESIC, AND GASTRIC TISSUE EFFECTS OF LACIDIPINE, ASPIRIN, AND THEIR COMBINATION
Isik, Bahar; Ates, Irem; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Gulaboglu, Mine; Ozcicek, Adalet; Suleyman, Halis
The increase in cyclooxygenase-2 (COX-2) activity and the decrease in COX-1 activity were associated with increased intracellular calcium. Lacidipine, a calcium channel blocker, can protect gastric tissue from aspirin-induced damage while potentiating the analgesic and anti-inflammatory properties of aspirin. The aim of this study was to investigate the anti-inflammatory, analgesic, and gastric tissue effects of using lacidipine and aspirin in combination and separately. (LA). Twenty-four rats were randomly divided into CG (carrageenan control), LCG (carrageenan + lacidipine), ACG (carrageenan + aspirin), and LACG (carrageenan + LA) groups. Lacidipine 4 mg/kg, aspirin 100 mg/kg were given orally to the animals on an empty stomach. Carrageenan was injected into the hind paws of rats to induce inflammation and pain. Paw volumes were measured at 0, 1, and 4 hours after carrageenan administration, and paw pain thresholds were measured at 1 and 4 hours. After euthanasia (thiopental sodium, 50 mg/kg), paw and gastric tissues were excised and biochemically analyzed. Gastric tissues were also examined macroscopically. In the paw tissues of animals receiving lacidipine, malondialdehyde (MDA) was lower than in the CG and AG, while total glutathione (tGSH) was higher (p<0.05). Lacidipine inhibited COX-2, but not COX-1 isoenzyme. LA—lacidipine, and aspirin—inhibited inflammation and hyperalgesia at 1 and 4 hours, respectively. Lacidipine prevented aspirin-induced COX-1 inhibition and gastric ulcer formation. Lacidipine combined with aspirin may be beneficial for initiating its anti-inflammatory activity early, achieving a potent analgesic effect, and preventing aspirin-induced gastric injury.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023The Role of Adrenaline, Noradrenaline, and Cortisol in the Pathogenesis of the Analgesic Potency, Duration, and Neurotoxic Effect of Meperidine
Yilmaz, Mehmet; Suleyman, Bahadir; Mammadov, Renad; Altuner, Durdu; Bulut, Seval; Suleyman, Halis
Background and Objectives: The purpose of the study was to investigate the role of adrenaline (ADR), noradrenaline (NDR), and cortisol in the pathogenesis of the analgesic potency, duration, and epilepsy-like toxic effect of meperidine. Materials and Methods: The experimental animals were separated into 11 groups of six rats. In the meperidine (MPD) and metyrosine + meperidine (MMPD) groups, paw pain thresholds were measured before and after the treatment between the first and sixth hours (one hour apart). In addition, ADR and NDR analyses were performed before and after the treatment, between the first and fourth hours (one hour apart). For the epilepsy experiment, caffeine, caffeine + meperidine, and caffeine + meperidine + metyrapone groups were created, and the treatment was applied for 1 day or 7 days. Groups were created in which caffeine was used at both 150 mg/kg and 300 mg/kg. Epileptic seizures were observed in epilepsy groups, latent periods were determined, and serum cortisol levels were measured. Results: In the MPD group, pain thresholds increased only at the first and second hours compared to pre-treatment, while ADR increased at the third hour, leading to a decrease in pain thresholds. In the MMPD group, the increase in paw pain thresholds at 1 and 6 h was accompanied by a decrease in ADR and NDR. In the caffeine (150 mg/kg) + meperidine group, 1-day treatment did not cause epileptic seizures, while seizures were observed and cortisol levels increased in the group in which treatment continued for 7 days. When cortisol levels were compared between the group in which caffeine (300 mg/kg) + meperidine + metyrapone was used for 7 days and the animals receiving caffeine (300 mg/kg) + metyrapone for 7 days, it was found that cortisol levels decreased and the latent period decreased. Conclusions: The current study showed that if serum ADR and cortisol levels are kept at normal levels, a longer-lasting and stronger analgesic effect can be achieved with meperidine, and epileptic seizures can be prevented.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effect of pycnogenol on ischemia/reperfusion-induced oxidative and inflammatory damage intheovariesof rats
Dinc, Kemal; Kiremitli, Sevil; Suleyman, Bahadir; Mammadov, Renad; Yavuzer, Bulent; Bulut, Seval; Yazici, Gulce N.; Coban, Taha A.; Altuner, Durdu; Suleyman, Halis
Purpose: To investigate the protective effect of pycnogenol (PYC) against ischemia/reperfusion (I/R) ovarian damage induced by experimental ovarian torsion in rats using biochemical and histopathological methods. Methods: Four groups of rats (n = 6) were randomly assigned and designated as follows - SG: sham group, PCG: pycnogenol (40 mg/kg) group, IRG: ovarian ischemia-reperfusion group, and PIR: pycnogenol (40 mg/kg) + ovarian ischemia-reperfusion group. In IRG and PYC treatment groups, ischemia was induced in the right ovary for two hours with vascular clips. The ovary was reperfused for two hours after ischemia was induced. Then, the levels of malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the ovarian tissues of rats were examined. Ovarian tissues were also examined histopathologically and follicle counts were performed. Results: Histopathological examination revealed that the developing follicles in ovary of I/R-induced group showed both morphological and cellular degeneration and vascular pathology. The PYC treatment group showed less ovarian damage, edema and vascular pathology than I/R-induced group (p < 0.05). The MDA, NF-κB, TNF-α and IL-1β levels in I/R-induced group were significantly higher than in SG and tGSH levels were significantly reduced by I/R damage (p < 0.05). Pycnogenol treatment reversed these biochemical indices as well as I/R-induced histopathological changes. Conclusion: Pycnogenol has a protective effect in rat ovaries by alleviating I/R-induced changes in biochemical parameters and histological disruptions. Further studies, including those in humans, to determine the effect of PYC on ovarian injuries would be required.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effect of Thymoquinone on Diclofenac-Induced Liver Injury
Ekinci, Bilge; Altuner, Durdu; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Suleyman, Zeynep; Gul, Mehmet A.; Ergul, Cetin; Suleyman, Halis
Background and Objective: Thymoquinone (TQ) is an active phenolic compound obtained from Nigella sativa L. It has anti-inflammatory and antioxidant activity by inhibiting the overproduction of certain inflammatory molecules and lipid peroxidation. TQ also has a hepatoprotective effect. This study, it was aimed to biochemically investigate the effect of TQ on diclofenac (DC)-induced liver damage in rats. Materials and Methods: The animals were divided into healthy control (HG), only diclofenac (DG), only thymoquinone (TQG) and diclofenac+thymoquinone (DTQG) groups. The DC was injected intraperitoneally at a dose of 25 mg kg(-1). The TQ was administered orally to the stomach at a dose of 20 mg kg(-1). This procedure was repeated once a day for 7 days. Results: Biochemical test results showed that TQ significantly prevented the increase in oxidant parameters and the decrease in antioxidants in liver tissue, which is formed by DC. Also, DC and TQ inhibited the increase of proinflammatory cytokines in liver tissue. The TQ also prevented the decrease of COX-1 activity by DC and increased the inhibition of COX-2. The TQ also significantly suppressed the elevation of liver function markers such as Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) with DC. Conclusion: These findings indicated that the hepatotoxic effect of DC was due to oxidative stress and inhibition of cytoprotective structural COX-1 enzyme. It suggested that TQ may be useful in the treatment of DC-related liver injury.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats
Ersoy, Alevtina; Tanoglu, Ceyda; Yazici, Gulce Naz; Coban, Taha Abdulkadir; Mammadov, Renad; Suleyman, Halis
Acrylamide is a neurotoxic compound. Moreover, anakinra is an interleukin-1 (IL-1) receptor antagonist used in rheumatoid arthritis treatment. This study investigated the effect of anakinra on acrylamide-related neuropathy and neuropathic pain. Acrylamide exposure caused a significant decrease in the pain threshold; an increase in malondialdehyde (MDA), tumor necrosis factor -alpha (TNF-alpha), and interleukin-1 beta (IL-113) levels; and a decrease in total glutathione (tGSH) values in the sciatic nerve. This indicates hyperalgesia presence, oxidative stress, and peripheral nerve tissue inflammation. Anakinra treatment significantly reduced the MDA, IL-113, and TNF-alpha levels, and increased the pain threshold and mean tGSH values. The analgesic effect of anakinra was 67.9% at the first hour, increasing to 74.9% and 76.7% at the second and third hours, respectively. The group receiving acrylamide exhibited histopathological changes (e.g., swollen and degenerated axons, hypertrophic and hyperplasic Schwann cells, and congested vessels). The use of anakinra significantly improved these morphological changes. Anakinra is concluded to reduce neuropathic pain and prevent neurotoxic effect of acrylamide on peripheral nerves due to its analgesic, antioxidant, and anti-inflammatory properties.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022The effect of rutin on pulmonary contusion induced by blunt trauma in rats: Biochemical and histopathological evaluation
Elma, Bekir; Mammadov, Renad; Bilgin, Yasin; Yazici, Gulce Naz; Süleyman, Halis; Çoban, Taha Abdulkadir
Background: This study aims to investigate the possible protective effects of rutin, also called vitamin P1, against pulmonary contusion induced by blunt chest trauma in a rat model. Methods: Thirty male albino Wistar rats were separated into three equal groups as healthy group, trauma group, and trauma+rutin group. After anesthesia provided by intraperitoneal administration of 60 mg/kg ketamine and xylazine by inhalation at appropriate intervals, 200 g weight was dropped from 1 m height to the anterior chest wall of the animals in the trauma group (n=10) and trauma+rutin group (n=10) and pulmonary contusion was created. Thirty min after the trauma, 50 mg/kg of rutin was administered into the stomach of trauma+rutin group animals orally with gavage. The rats received rutin once daily for two days and were sacrificed 48 h later. Their lung tissues were removed and examined biochemically and histopathologically. Results: Nuclear factor-kappa B, cyclooxygenase-2, and malondialdehyde levels increased in the trauma group compared to the healthy group, and rutin administration prevented this increase. Total glutathione levels decreased in the trauma group, and rutin administration also prevented this decrease. The histopathological findings were compatible with the biochemical findings. Conclusion: Our study results suggest that rutin has a protective effect on contused lung tissue in rats.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation
Tanoğlu, Ceyda; Ersoy, Alevtina; Çoban, Taha Abdulkadir; Yazıcı, Gülce Naz; Mammadov, Renad; Süleyman, Bahadır
Cobalt is a trace element that increases lipid peroxidation and malondialdehyde levels and reduces the antioxidant defense mechanisms of nerve cells. High levels of cobalt exposure may cause peripheral neuropathy, but the mechanism behind this has not yet been elucidated. Taxifolin is a flavonoid whose antioxidant and anti-inflammatory properties are well-known. We aimed to investigate the effect of taxifolin on cobalt-induced oxidative sciatic nerve damage. Eighteen albino male Wistar rats were assigned to three groups: Control, Cobalt, and Taxifolin + Cobalt groups. Total oxidant and total antioxidant status and levels of malondialdehyde, total glutathione, and superoxide dismutase were measured to determine the effect of taxifolin on cobalt-induced sciatic nerve injury. The following statistically significant effect of taxifolin was observed: It prevented cobalt-induced oxidative sciatic nerve damage by reducing malondialdehyde levels and total oxidant status and increasing total antioxidant status, total glutathione levels, and superoxide dismutase levels. In a histopathological analysis, we observed similar findings in Control and Taxifolin + Cobalt groups. We determined that taxifolin is effective in preventing cobalt-induced oxidative damage in sciatic nerve injury.
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