Department of Pharmacology, Cardiovascular Research Laboratory, All India Institute of Medical Sciences, New Delhi, India.
Department of Pathology, All India Institute of Medical Sciences, New Delhi-110029, India.
Curr Mol Pharmacol. 2020;13(4):342-352. doi: 10.2174/1874467213666200220142202.
The activation of Nrf2/HO-1 pathway has been shown to protect against cisplatin- induced nephrotoxicity by reducing oxidative stress. Berberine (Ber), an isoquinoline alkaloid, has demonstrated antioxidant, anti-inflammatory and anti-apoptotic activities in various experimental models.
To check the effect of Ber on cisplatin-induced nephrotoxicity and to explore the involved mechanism.
Adult male Wistar rats were divided into 6 groups: Normal, cisplatin-control, treatment groups and per se group. Normal saline and Ber (20, 40 and 80 mg/kg; p.o.) was administered to rats for 10 days. A single intraperitoneal injection of cisplatin (8 mg/kg) was injected on 7th day to induced nephrotoxicity. On 10th day, rats were sacrificed, the kidney was removed and stored for the estimation of various parameters.
As compared to cisplatin-control group, Ber pretreatment improved renal function system and preserved renal architecture. It also diminished oxidative stress by upregulating the expression of Nrf2/HO-1 proteins. In addition, Ber attenuated the cisplatin mediated inflammation and apoptosis. Furthermore, it also reduced the phosphorylation of p38/JNK and PARP/Beclin-1 expression in the kidney.
Ber attenuated renal injury by activating Nrf2/HO-1 and inhibiting JNK/p38MAPKs/ PARP/Beclin-1 expression which prevented oxidative stress, inflammation, apoptosis and autophagy in renal tissue.
Nrf2/HO-1 通路的激活已被证明通过减少氧化应激来保护顺铂诱导的肾毒性。小檗碱（Ber）是一种异喹啉生物碱，在各种实验模型中表现出抗氧化、抗炎和抗凋亡活性。
检查 Ber 对顺铂诱导的肾毒性的影响，并探讨其涉及的机制。
将成年雄性 Wistar 大鼠分为 6 组：正常组、顺铂对照组、治疗组和自身组。正常生理盐水和 Ber（20、40 和 80mg/kg；po）连续 10 天给予大鼠。第 7 天单次腹腔注射顺铂（8mg/kg）诱导肾毒性。第 10 天，处死大鼠，取出肾脏，用于估计各种参数。
与顺铂对照组相比，Ber 预处理改善了肾功能系统并保存了肾脏结构。它还通过上调 Nrf2/HO-1 蛋白的表达来减少氧化应激。此外，Ber 还减弱了顺铂介导的炎症和细胞凋亡。此外，它还降低了肾脏中 p38/JNK 和 PARP/Beclin-1 表达的磷酸化。
Ber 通过激活 Nrf2/HO-1 并抑制 JNK/p38MAPKs/PARP/Beclin-1 表达来减轻肾损伤，从而防止肾组织中的氧化应激、炎症、凋亡和自噬。
