Kumar Raushan, Arya Jitendra Kumar, Rizvi Syed Ibrahim
Department of Biochemistry, University of Allahabad, Allahabad, 211002, India.
Mol Biol Rep. 2022 Oct;49(10):9465-9472. doi: 10.1007/s11033-022-07810-6. Epub 2022 Aug 4.
An altered lipid profile may lead to the development of inflammation and NAFLD (Non-alcoholic fatty liver disease). Although statins have a positive effect on blood lipid levels their long-term use is known to cause adverse effects, in this backdrop there is an interest in natural compounds which may affect lipid metabolism and prevent NAFLD. We have examined the effect of Chitosan on rats subjected to a high-fat diet.
Male Wistar middle aged rats (12-16 months) were treated with high-fat diet orally for two months for creating a NAFLD model. Rats were also supplemented with Chitosan (2% chitosan daily) for 2 months. We assessed the activity of antioxidant enzymes, the histopathological profile of the liver. Inflammatory cytokines and adiponectin levels were also measured in serum. HFD induced significant changes in liver tissue and inflammatory markers (Il-6, TNF- alpha, NF-KB). Chitosan treatment protected rats from HFD induced alterations.
The findings suggest that Chitosan can effectively improve liver lipid metabolism by normalizing cholesterol, triglyceride, lowering NF-KB expression, and protecting the liver from oxidative stress by improving hepatic function. Chitosan also regulates genes related to lipidemic stress i,e leptin and adiponectin.
脂质谱改变可能导致炎症和非酒精性脂肪性肝病（NAFLD）的发生。尽管他汀类药物对血脂水平有积极影响，但长期使用已知会产生不良反应，在此背景下，人们对可能影响脂质代谢并预防NAFLD的天然化合物产生了兴趣。我们研究了壳聚糖对高脂饮食大鼠的影响。
雄性中年Wistar大鼠（12 - 16个月）经口给予高脂饮食两个月以建立NAFLD模型。大鼠同时补充壳聚糖（每日2%壳聚糖），持续2个月。我们评估了抗氧化酶的活性、肝脏的组织病理学特征。还测定了血清中的炎性细胞因子和脂联素水平。高脂饮食诱导肝脏组织和炎性标志物（白细胞介素-6、肿瘤坏死因子-α、核因子-κB）发生显著变化。壳聚糖治疗可保护大鼠免受高脂饮食诱导的改变。
研究结果表明，壳聚糖可通过使胆固醇、甘油三酯正常化，降低核因子-κB表达，并通过改善肝功能保护肝脏免受氧化应激，从而有效改善肝脏脂质代谢。壳聚糖还调节与脂质代谢应激相关的基因，即瘦素和脂联素。
