Department of Physiology (UG & PG), Serampore College, 9 William Carey Road, Serampore, Hooghly-712201, West Bengal, India.
Department of Physiology, University College of Science, Technology and Agriculture, University of Calcutta, 92 Acharya Prafulla Chandra Road, Kolkata-700009, West Bengal, India.
Sci Rep. 2020 Sep 22;10(1):15443. doi: 10.1038/s41598-020-72076-6.
In the context of failure of treatment for non alcoholic fatty liver disease (NAFLD)-mediated systemic damages, recognition of novel and successful characteristic drug to combat these anomalous situations is earnestly required. The present study is aimed to evaluate protective value of ethanol extract of Coccinia grandis leaves (EECGL), naturally occurring medicinal plant, on NAFLD-mediated systemic damage induced by high lipid diet along with monosodium glutamate (HM)-fed rats. Our study uncovered that EECGL significantly ameliorates HM-induced hyperlipidemia, increased lipogenesis and metabolic disturbances (via up regulation of PPAR-α and PPAR-γ), oxidative stress (via reducing the generation of reactive oxygen species and regulating the redox-homeostasis) and inflammatory response (via regulating the pro-inflammatory and anti-inflammatory factors with concomitant down regulation of NF-kB, iNOS, TNF-α and up regulation of eNOS). Furthermore, EECGL significantly inhibited HM-induced increased population of cells in sub G0/G1 phase, decreased Bcl2 expression and thereby loss of mitochondrial membrane potential with over expression of Bax, p53, p21, activation of caspase 3 and 9 indicated the apoptosis and suppression of cell survival. It is perhaps the first comprehensive study with a mechanistic approach which provides a strong unique strategy for the management of HM-induced systemic damage with effective dose of EECGL.
在非酒精性脂肪性肝病(NAFLD)介导的全身损害治疗失败的情况下,迫切需要认识到新型有效的特色药物来对抗这些异常情况。本研究旨在评估天然药用植物大籽雪胆叶乙醇提取物(EECGL)对高脂肪饮食加单谷氨酸钠(HM)喂养大鼠诱导的 NAFLD 介导的全身损害的保护作用。我们的研究表明,EECGL 可显著改善 HM 诱导的高脂血症、增加脂肪生成和代谢紊乱(通过上调 PPAR-α 和 PPAR-γ)、氧化应激(通过减少活性氧的产生和调节氧化还原平衡)和炎症反应(通过调节促炎和抗炎因子,同时下调 NF-kB、iNOS、TNF-α和上调 eNOS)。此外,EECGL 显著抑制 HM 诱导的 G0/G1 期细胞数量增加,降低 Bcl2 表达,从而导致线粒体膜电位丧失,Bax、p53、p21 过表达,caspase 3 和 9 激活,表明细胞凋亡和抑制细胞存活。这或许是第一项具有机制研究方法的全面研究,为 HM 诱导的全身损害提供了一种有效的 EECGL 治疗策略。