مقالات پذیرفته شده در هفتمین کنگره بین المللی زیست پزشکی
Investigating the effect of curcumin on cisplatin-induced pancreatic toxicity in rats
Investigating the effect of curcumin on cisplatin-induced pancreatic toxicity in rats
Nilufar lotfian,1Zeinab Shafiei,2Dian Dayer,3Vahid Bayati,4Esrafil Mansouri,5,*
1. Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran 2. Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran 3. Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran 4. Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran 5. Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Introduction: Cisplatin (CP) is an influential chemotherapeutic agent in the treatment of several types of malignant solid tumors, but its clinical use is related to pancreas toxicity. curcumin (CUR) is a natural antioxidant and scavenging free radicals. Here, we first explore the efficacy of CUR in the pancreas against the toxicity of CP and also analyze its mechanism.
Methods: Twenty-four Sprague-Dawley rats were equally divided into 3 groups, including, the control group which received only normal saline; the CP group which received only one dose CP (7 mg/kg/day) intraperitoneally (i.p.) for 24 h, groups treated with doses of 200 mg/kg/day CUR i.p. for 7 days, and the group treated which received the same dose of CP with doses of 200 mg/kg/day CUR i.p. for 7 days. After the treatments, animals were sacrificed. The malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels were evaluated in the pancreas. The histopathology of the pancreas was examined using hematoxylin-eosin. The serum was provided to assess Inflammatory factor (tumor necrosis factor (TNF)-alpha) and the lipase and amylase values.
Results: The results showed that CP significantly increased the level of MDA in tissue as compared to the control group. Moreover, severe tissue damage was detected in the pancreas. Whereas CUR significantly decreased the level of MDA. The activities of CAT, GSH-Px, and SOD in the pancreas tissues of the rats injected with CP were significantly lower than their activities in the control group. However, treatment with CUR in animals co-treated with CP resulted in a significant increase in the activities of pancreas tissues, when compared to the CP-treated group. In the CP group, the levels of amylase and lipase increased compared with the control group. However, there were statistically significant differences among the CP group and the CP+ CUR groups in the values of both amylase and lipase. Serum TNF-alpha concentration in the CP+ CUR group significantly decreased compared with that in the cisplatin group. In addition, histopathological findings observed in the CP group in the pancreatic tissue alleviated in CP+ CUR groups.
Conclusion: These results indicate that curcumin acts to reduce cisplatin-induced pancreatic toxicity through its anti-inflammatory effects. Thus, curcumin may become a new therapeutic candidate for the treatment of cisplatin-induced pancreatic toxicity.