YNCRG通过改善脂质代谢和慢性炎症反应减轻代谢综合征模型大鼠肝脂肪变性

Bo-ju Sun, Maya Kudo, Misa Hayashi, Lingling Qin, Lili Wu, Tonghua Liu, Ming Gao
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摘要

YNCRG是由五种具有药用特性的中药成分组合而成。我们研究了它对伴有代谢综合征的非酒精性脂肪肝大鼠模型的作用及其作用机制。将8周龄雄性SHRcp大鼠和Wister Kyoto(WKY)大鼠适应性喂养1周后,随机分为三组,包括对照组(n=9)、YNCRG组(n=8)和WKY组(n=8)。WKY组可自由饮水,对照组每天饮水,YNCRG组灌胃YNCRG水溶液(3.6g/kg体重/天)8周。干预8周后,与对照组大鼠的体重相比,YNCRG有效降低了大鼠的重量,并显著降低了血清AST、ALT、CHO和TG水平。RT-PCR结果显示,NF-κB、TLR4、TNF-α和IL-1β的mRNA水平升高,MCP-1和ICAM-1的水平也升高,但YNCRG有效降低了mRNA水平。Western印迹分析结果表明,YNCRG不影响AMPK/ACC信号通路,但强烈促进大鼠肝脏PKA、ERK和C/EBPβ的磷酸化。YNCRG也显著促进IRS-1的磷酸化(Tyr465),但抑制IRS-1(Ser1101);两者都是ERK的上游因素。我们发现YNCRG可以减少代谢综合征大鼠肝脏中脂质的积累,可能是通过影响脂质代谢和与炎症反应相关的信号通路。
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YNCRG Alleviated Hepatic Steatosis in Metabolic Syndrome Model Rats by Improving Lipid Metabolism and Chronic Inflammatory Reaction
YNCRG is a combination of five traditional Chinese ingredients with medicinal properties. We studied its effects and mechanism of action on a rat model of non-alcoholic fatty liver with metabolic syndrome. Eight-week-old male SHRcp rat(s) and Wister Kyoto (WKY) rats were adaptively fed for one week, after which they were randomly divided into three groups, including the control group (n = 9), the YNCRG group (n = 8), and the WKY group (n = 8). The WKY group could freely consume water, the control group was provided water every day, and the YNCRG group was gavaged with an aqueous solution of YNCRG (3.6 g/kg body weight/day) for eight weeks. After eight weeks of intervention, YNCRG effectively reduced the weight of rats and significantly reduced the serum levels of AST, ALT, CHO, and TG compared to the weight of the rats in the control group. The RT-PCR results showed that mRNA levels of NF-κB, TLR4, TNF-α, and IL-1β increased, and the levels of MCP-1 and ICAM-1 also increased, but YNCRG effectively reduced the mRNA levels. The results of the Western blotting assay showed that YNCRG did not affect the AMPK/ACC signaling pathway, but it strongly promoted the phosphorylation of PKA, ERK, and C/EBPβ in rat livers. YNCRG also significantly promoted the phosphorylation of IRS-1 (Tyr465) but inhibited IRS-1 (Ser1101); both are upstream factors of ERK. We found that YNCRG can reduce the accumulation of lipids in the liver of rats with metabolic syndrome, probably by affecting lipid metabolism and the signaling pathway associated with inflammatory reactions.
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