Toxicology and Pharmacology Laboratory, Department of Zoology Guru Ghasidas University, Bilaspur, 495009 (C.G.), India.
Laboratory of Natural Products, Department of Rural Technology and Social Development Guru Ghasidas University, Bilaspur 495009 (C.G.), India.
Curr Pharm Biotechnol. 2020;21(14):1489-1504. doi: 10.2174/1389201021666200615165732.
Secondary metabolites of plants, the polyphenols, play a vital role in protection from many health problems in human beings. Structurally favored phytochemicals may be studied to protect multiorgan injury. At pharmacological doses, gallic acid is nontoxic to mammals and is generally absorbed in the intestine.
In this present study, gallic acid was evaluated for its protective efficacy against Lipo Polysaccharide (LPS) and d-Galactosamine (D-GalN) induced multiorgan injury, i.e., liver, kidney and brain.
Three different doses of gallic acid (5, 10 and 20 mg/kg p.o.) were administered to the experimental animals for 6 consecutive days, followed by exposure to LPS (50 μg/kg I.P.) and D-GalN (300 mg/kg I.P.) on the 6th day.
Exposure to LPS and D-GalN resulted in increased oxidative stress and proinflammatory cytokines. Altered hematology and serology due to LPS and D-GalN were restored towards control by gallic acid. Declined antioxidants such as reduced glutathione, superoxide dismutase and catalase due to injurious effects of LPS and D-GalN were rejuvenated by gallic acid.
Exposure to LPS and D-GalN severely increased lipid peroxidation, CYP2E1 activity and tissue lipids while lowered protein content. Gallic acid restored all these parameters towards control in dose dependent manner and 20 mg/kg dose provided the best protection. Histological study showed improved histoarchitecture of liver, kidney and brain that supported biochemical endpoints.
Gallic acid minimized oxidative stress and provided best protection at 20 mg/kg dose against LPS and D-GalN induced multi organ acute injury.
植物的次生代谢产物多酚在保护人类免受许多健康问题方面起着至关重要的作用。结构上有利的植物化学物质可以被研究来保护多器官损伤。在药理剂量下，没食子酸对哺乳动物无毒，通常在肠道中被吸收。
在本研究中，评估了没食子酸对脂多糖（LPS）和 D-半乳糖胺（D-GalN）诱导的多器官损伤（即肝、肾和脑）的保护作用。
三种不同剂量的没食子酸（5、10 和 20 mg/kg，po）连续 6 天给予实验动物，然后在第 6 天暴露于 LPS（50 μg/kg，ip）和 D-GalN（300 mg/kg，ip）。
暴露于 LPS 和 D-GalN 导致氧化应激和促炎细胞因子增加。LPS 和 D-GalN 引起的血液学和血清学改变通过没食子酸恢复到对照水平。由于 LPS 和 D-GalN 的损伤作用，抗氧化剂如还原型谷胱甘肽、超氧化物歧化酶和过氧化氢酶下降，通过没食子酸得到恢复。
暴露于 LPS 和 D-GalN 严重增加了脂质过氧化、CYP2E1 活性和组织脂质，同时降低了蛋白质含量。没食子酸以剂量依赖性方式将所有这些参数恢复到对照水平，20mg/kg 剂量提供了最佳保护。组织学研究显示，肝脏、肾脏和大脑的组织形态学得到改善，支持了生化终点。
没食子酸最大限度地减少了氧化应激，并在 20mg/kg 剂量下提供了针对 LPS 和 D-GalN 诱导的多器官急性损伤的最佳保护。
