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传统复方草药通过抑制氧化应激和 MAPK 信号通路对顺铂诱导的急性肾损伤细胞模型的保护作用。

Protective Effects of Traditional Polyherbs on Cisplatin-Induced Acute Kidney Injury Cell Model by Inhibiting Oxidative Stress and MAPK Signaling Pathway.

机构信息

Department of Anatomy and Histology, College of Korean Medicine, Daegu Haany University, Gyeongsan 38610, Korea.

Research Center for Herbal Convergence on Liver Disease, College of Korean Medicine, Daegu Haany University, Gyeongsan 38610, Korea.

出版信息

Molecules. 2020 Nov 30;25(23):5641. doi: 10.3390/molecules25235641.

Abstract

Acute kidney injury (AKI) is a disease caused by sudden renal dysfunction, which is an important risk factor for chronic renal failure. However, there is no effective treatment for renal impairment. Although some traditional polyherbs are commercially available for renal diseases, their effectiveness has not been reported. Therefore, we examined the nephroprotective effects of polyherbs and their relevant mechanisms in a cisplatin-induced cell injury model. Rat NRK-52E and human HK-2 subjected to cisplatin-induced AKI were treated with four polyherbs, Injinhotang (IJ), Ucha-Shinki-Hwan (US), Yukmijihwang-tang (YJ), and Urofen (Uro) similar with Yondansagan-tang, for three days. All polyherbs showed strong free radical scavenging activities, and the treatments prevented cisplatin-induced cell death in both models, especially at 1.2 mg/mL. The protective effects involved antioxidant effects by reducing reactive oxygen species and increasing the activities of superoxide dismutase and catalase. The polyherbs also reduced the number of annexin V-positive apoptotic cells and the expression of cleaved caspase-3, along with inhibited expression of mitogen-activated protein kinase-related proteins. These findings provide evidence for promoting the development of herbal formulas as an alternative therapy for treating AKI.

摘要

急性肾损伤 (AKI) 是由肾功能突然丧失引起的疾病,是慢性肾衰竭的重要危险因素。然而,对于肾损伤还没有有效的治疗方法。尽管一些传统的草药在商业上可用于肾脏疾病,但它们的有效性尚未得到报道。因此,我们在顺铂诱导的细胞损伤模型中研究了草药的肾保护作用及其相关机制。用四种草药(IJ、US、YJ 和 Uro)处理顺铂诱导的 AKI 大鼠 NRK-52E 和人 HK-2 细胞,类似于 Yondansagan-tang 的处理,持续三天。所有草药均显示出很强的自由基清除活性,并且这些治疗在两种模型中均能预防顺铂诱导的细胞死亡,尤其是在 1.2mg/mL 时。保护作用涉及通过减少活性氧和增加超氧化物歧化酶和过氧化氢酶的活性来发挥抗氧化作用。草药还减少了 annexin V 阳性凋亡细胞的数量和 cleaved caspase-3 的表达,并抑制了丝裂原激活蛋白激酶相关蛋白的表达。这些发现为促进草药配方的开发提供了证据,作为治疗 AKI 的替代疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db46/7730198/11a8332e7fad/molecules-25-05641-g001.jpg

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