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) 介导的全身性损伤治疗失败的情况下，迫切需要识别新的和成功的特征药物来对抗这些异常情况。本研究旨在评价大红球藻乙醇提取物的保护价值。叶 (EECGL)，天然存在的药用植物，对高脂饮食和谷氨酸钠 (HM) 喂养的大鼠引起的 NAFLD 介导的全身性损伤的影响。我们的研究发现 EECGL 显着改善 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稳态）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 显着抑制 HM 诱导的亚 G0/G1 期细胞群增加，降低 Bcl2 表达，从而随着 Bax、p53、p21、caspase 3 和 9 的激活表明细胞凋亡和细胞存活受到抑制。这可能是第一个采用机械方法的综合研究，它为使用有效剂量的 EECGL 管理 HM 引起的全身性损伤提供了强大的独特策略。