Erkan, Hirik; Aliseydi, Bozkurt; Keskin, Ercument; Abdullah, Erdogan; Ali, Gul Mehmet; Halis, Suleyman; Zeynep, Suleyman

Rutin (Vitamin P1) is an antioxidant and anti-inflammatory flavonoid. This study examined the effect of rutin on the potential of cisplatin to cause oxidative and proinflammatory damage in blood serum, ureter, bladder and urethra in rats. Animals were divided into four groups: (i) healthy (HG), (ii) 50 mg/kg of rutin + 5 mg/kg of cisplatin (C + R50), (iii) 100 mg/kg of rutin + 5 mg/kg of cisplatin (C + R100) and (iv) only cisplatin (CG). Rutin and distilled water were applied once a day for eight days. Cisplatin was injected intraperitoneally at a dose of 5 mg/kg for eight days, once every two days. Finally, animals were sacrificed by high -dose anesthesia after blood samples were taken. Ureter, bladder and urethra tissues were removed and malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), superoxide dismutase (SOD) interleukin beta (IL-1β) and tumor necrosis factor alpha (TNF-α) levels were measured. The results showed that the levels of MDA, MPO, IL-1β and TNF-α in the blood serum of the CG group increased significantly (p < 0.0001) and the tGSH and SOD levels decreased compared to the HG. Rutin administration reversed the effect as seen in C + R50 and C + R100 groups. However, there was no statistically significant difference in the levels of MDA, MPO, tGSH, SOD, IL-1β and TNF-α in ureter, bladder and urethra tissue (p > 0.05).This suggests that cisplatin produces oxidative stress in the blood serum but not in the ureter, bladder and urethra tissues. It was observed that rutin prevented the cisplatin-related oxidative and proinflammatory damage in the blood serum.

Cimen, Orhan; Eken, Hüseyin; Keskin Cimen, Ferda; Ozbek Bilgin, Asli; Pehlivanoglu, Kamil; Kurnaz, Eray; Gülaboglu, Mine; Suleyman, Bahadir; Suleyman, Halis

Ischemia reperfusion (IR) injury is defined as a pathological process which initiates with tissue deoxygenation, continues with oxidative stress, and spreads with inflammation. Increased intracellular calcium is responsible for oxidative stress and inflammation during this process. Benidipine is an antihypertensive drug acting as an T/L-type calcium channel blocker. The effect of benidipine on cyclooxygenase-2 (COX-2) activity is not known. Benidipine being a calcium channel blocker suggests that it may suppress oxidant and proinflammatory COX-2 production. The aim of this study was to examine the effect of benidipine on IR induced liver injury in albino Wistar male rats. Animals were divided into three groups: liver ischemia reperfusion (LIR), 2 mg/kg benidipine + liver ischemia reperfusion (BLIR), and sham surgery (SHAM). Hepatic artery, portal vein and bile duct were clamped to obtain ischemia for one hour and reperfusion for six hours. Malondialdehyde (MDA), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and COX-2 levels were higher, whereas total glutathione (tGSH) and cyclooxygenase-1 (COX-1) levels were lower in the LIR group. Liver tissue of the LIR group showed marked dilated congested blood vessels and increased bile duct proliferation, polymorphonuclear leukocyte infiltration, edema, hemorrhage and destruction. MDA, ALT, AST and COX-2 levels were lower, and tGSH and COX-1 levels were higher in the BLIR group treated with benidipine. Liver tissue of the BLIR group was found to be normal except for mild dilated blood vessels. These experimental findings indicate that benidipine may be useful in the treatment of liver IR injury.