Nephroprotective Effects of Anthocyanin from the Fruits of Panax ginseng (GFA) on Cisplatin‐Induced Acute Kidney Injury in Mice

• DOI: 10.1002/ptr.5867
• Publication Date: 2017-07-21T09:33:05Z
• Authors: Zhen‐Lan Qi; Zi Wang; Wei Li; Jin‐Gang Hou; Ying Liu; Xin‐Dian Li; Hui‐Ping Li; Ying‐Ping Wang
• Keywords: Male; 0301 basic medicine; Mice, Inbred ICR; Anti-Inflammatory Agents; Panax; Antineoplastic Agents; Acute Kidney Injury; Kidney; 3. Good health; Anthocyanins; Mice; Oxidative Stress; 03 medical and health sciences; Fruit; Animals; Cisplatin

Cisplatin is an effective anticancer chemotherapeutic agent, but the use of cisplatin in the clinic is severely limited by side effects. Nephrotoxicity is a major factor that contributes to the side effects of cisplatin chemotherapy. The aim of this research was to survey the nephroprotective effects of anthocyanin from the fruits of Panax ginseng (GFA) in a murine model of cisplatin‐induced acute kidney injury. We observed that pretreatment with GFA attenuated cisplatin‐induced elevations in blood urea nitrogen and creatinine levels and histopathological injury induced by cisplatin. The formation of kidney malondialdehyde, heme oxygenase‐1, cytochrome P450 E1 and 4‐hydroxynonenal with a concomitant reduction in reduced glutathione was also inhibited by GFA, while the activities of kidney superoxide dismutase and catalase were all increased. GFA also inhibited the increase in serum tumour necrosis factor‐α and interleukin‐1β induced by cisplatin. In addition, the levels of induced nitric oxide synthase and cyclooxygenase‐2 were suppressed by GFA. Furthermore, GFA supplementation inhibited the activation of apoptotic pathways by increasing B cell lymphoma 2 and decreasing Bcl2‐associated X protein expression. In conclusion, the findings from the present investigation demonstrate that GFA pre‐administration can significantly prevent cisplatin‐induced nephrotoxicity, which may be related to its antioxidant, anti‐apoptotic and antiinflammatory effects. Copyright © 2017 John Wiley & Sons, Ltd.