Study On The Effect And Mechanism Of Matcha On High-Fat Induced Hepatic Inflammation And Liver Cancer

Obesity is a major causative factor of cardiovascular disease,type 2 diabetes,fatty liver,hypertension,hyperlipidemia and other related metabolic syndrome,which poses a very serious threat to people's health.Searching for safe and effective treatment methods for improving obese conditions has become a research hotspot in recent years.Tea has been reported to have strong health effects of improving obesity,sterilizing anti-inflammatory,anti-cancer and anti-radiation.Matcha is a traditional Chinese drink,its use of “eating tea” makes the full use of all functional ingredients in tea and has outstanding health research value in the utilization of functional ingredients.Matcha has been reported to improve blood sugar and intestinal flora,protect against kidney and liver damage caused by type 2 diabetes,and ameliorate obesity and related complications.However,the specific molecular mechanism behind these effects still needs further exploration.This paper studied the effects of Matcha on high fat diet induced obesity,lipid accumulation,hepatitis reaction and liver cancer.Through the related cell models and animal models,the efficacy and regulation mechanism of Matcha to improve obesity and protect liver damage were studied.The main findings of this paper are as follows:(1)Matcha water extract(MWE)and matcha ethanol extract(MEE)were prepared by water leaching and 70% ethanol extraction.The content of biochemical components such as free amino acids,tea polyphenols,catechin,caffeine,total sugar,and soluble protein in MWE and MEE were determined.It was found that both MWE and MEE were rich in tea polyphenols and EGCG.In addition,MWE contains more free amino acids and total sugars,and MEE contains more tea polyphenols,proteins and caffeine.In terms of antioxidant activity,both showed good DPPH scavenging ability,ABTS scavenging ability and iron ion reducing ability.Overall,MEE was stronger than MWE.(2)We established a human liver L0-2 cell model induced by palmitic acid and observed the effect of MEE and MWE on morphological changes and inflammatory responses of L0-2 cells.It could be seen from the experimental results that Matcha extract can improve the morphological damage and reduce lipid accumulation of L0-2 cells under PA stimulation in a concentrationdependent manner.At the same time,palmitic acid-induced TNF-? inflammatory factor release and TLR4 and MyD88 protein expression were decreased to some extent,indicating that the inhibition of high-fat-induced hepatic inflammatory injury by Matcha may be closely related to the inhibition of TLR4/MyD88 pathway activation.(3)We established a high-fat diet-induced obese mouse model.Fifty C57BL/6 mice were devided into five groups,fed a normal diet,a high-fat diet,a high-fat diet supplemented with 0.1% Matcha,a high-fat diet supplemented with 0.5% Matcha and a high-fat diet with 1.0% Matcha.Obesity-related characterization and hepatic inflammatory response were observed after 6 weeks of feeding.Results showed that dietary supplemented Matcha could significantly reduce the body weight gain,fat cell accumulation,blood glucose and lipid increase and abnormal increase of inflammatory cytokines in liver tissue caused by high-fat diet.In addition,PCR and WB assays of TLR4 and MyD88 in liver tissues showed that Matcha can inhibit TLR4 and MyD88 expression,indicating that TLR4/MyD88 signaling pathway is a potential target for Matcha to inhibit liver inflammatory response induced by high fat diet.(4)In this paper,the anti-hepatocarcinoma effect of MEE and MWE was studied through human hepatoma cell HepG2 model.Results showed that Matcha extract could inhibit the proliferation and migration of HepG2 cells in a concentration-dependent manner and promote cell apoptosis and cell cycle arrest.Overall,MEE was superior to MWE.Matcha extract could also increase the levels of cellular antioxidant enzymes SOD,CAT and GSH.Results of WB experiment on key factors of related pathways showed that Matcha extract decreased the expression of Bcl-2,a key factor related to apoptosis,increase the expression of Bax,and decrease the ratio of Bcl-2/Bax,thus promoting the apoptosis of HepG2 cells.