Effect and Mechanism of Carvacrol on Liver Injury in Type 2 Diabetes Mellitus
Objective To observe the protective effect of carvacrol on liver injury in type 2 diabetes mellitus(T2DM)mice and explore its possible molecular mechanism from the perspective of Toll-like receptor 4(TLR4)/nuclear factor kappa-B(NF-κB)and protein kinase B1(AKT1)/mammalian target of rapamycin(mTOR)signaling pathways.Methods Spontaneous type 2 diabetic db/db mice were randomly divided into model group and carvacrol group,and db/m mice were set as normal control group.After 6 weeks of administration,fasting blood glucose(FBG)was detected in mice.Fasting insulin,glycated serum protein(GSP),aspartate transaminase(AST),alanine aminotrans(ALT),high density lipoprotein cholesterol(HDL-C),total cholester-ol(TC),triglyceride(TG)and low density lipoprotein cholesterol(LDL-C)were detected by ELISA.Hematoxylin-eosin stai-ning(HE)and periodic acid-Schiff staining(PAS)were used to observe the pathological changes of liver tissue.Western Blot was used to detect the expressions of TLR4,NF-KB,Nod-like receptor protein 3(NALP3),AKT1,phospho-protein kinase B1(p-AKT1),Iusulin receptor(INSR),phospho-Iusulin receptor substrate1(p-IRS1),mTOR,phospho-mammalian tar-get of rapamycin(p-mTOR),Iusulin receptor substrate1,(IRS1)and phospho-Iusulin receptor substrate1(p-IRS1)in liver tissue of mice.Results The levels of fasting blood glucose,GSP,AST,ALT,TC,LDL-C,TG,TLR4,NF-κB,NALP3,INSR,p-INSR,IRS 1 and p-IRS1 in the carvacrol group were significantly decreased(P＜0.05),and the level of HDL-C was signifi-cantly increased(P＜0.05).The pathological damage of liver tissue in the carvacrol group was significantly reduced compared with those of the model group.Conclusion Carvacrol has a protective effect on liver injury in T2DM mice,and its mechanism may be related to the inhibition of TLR4/NF-κB and ATK1/mTOR inflammatory signaling pathways.
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