AIM:This study aimed to investigate the differences in hepatic lipid metabolites in ICR mice in-duced by a high-fat diet and treated with Shaqi concentrated pills(SQ).METHODS:Thirty 8-week-old SPF-grade ICR mice were randomly assigned to five groups:the normal(CON,n=6)group,the high-fat diet model(HFD,n=6)group,the low-dose SQ administration(SQL,n=6)group,the high-dose SQ administration(SQH,n=6)group,and the liver-protecting tablets positive control(PLT,n=6)group.The HFD group was fed a diet consisting of 60%fat for 8 weeks to es-tablish a metabolic-dysfunction-associated fatty liver disease model.Upon successful model establishment,the SQL group received a daily gavage of 395 mg/kg for 4 weeks,while the SQH group received 790 mg·kg-1·d-1.The PLT group was ad-ministered liver-protecting tablets at a dosage of 0.655 g/kg via gavage.Body weight and food intake were monitored week-ly.Liver indices,including Lee's index,triglyceride(TG),total cholesterol(TC),high-density lipoprotein cholesterol(HDL-C),low-density lipoprotein cholesterol(LDL-C),alanine aminotransferase(ALT),and aspartate transaminase(AST)levels,were measured in each group.Hematoxylin-eosin(HE)staining and oil red O staining were performed to assess the extent of pathological damage in liver tissues.Western blot analysis was conducted to evaluate the protein expres-sion levels of choline/ethanolamine phosphotransferase-1(CEPT1),adipose triglyceride lipase(ATGL),and diacylglycerol acyltransferase(DGAT)in the liver.A non-targeted lipidomic analysis using LC-MS was employed to detect changes in hepatic lipid content,and multivariate statistical analyses(principal component analysis and orthogonal partial least squares discriminant analysis)were utilized to compare lipid metabolic profiles among the groups and identify differential lipid metabolites.RESULTS:Compared to the CON group,mice in the HFD group exhibited significantly increased body weight,blood glucose levels,serum TG,TC,LDL-C,ALT,and AST levels,accompanied by a marked decrease in HDL-C levels.HE and oil red O staining results revealed significant lipid droplet accumulation in the liver tissues of HFD mice.In contrast,mice in the SQL and SQH groups showed significant reductions in body weight,blood glucose,serum TG,TC,LDL-C,ALT,and AST levels,along with increased HDL-C levels and less lipid accumulation in liver tissues compared to the HFD group.Staining of liver sections confirmed that SQ treatment mitigated the abnormal accumulation of lipid droplets.Lipidomic analysis indicated that SQ treatment normalized 25 aberrantly expressed lipid metabolites to lev-els comparable to the CON group and identified nine representative differential lipid metabolites.Western blot results dem-onstrated that SQ treatment reduced the protein expression levels of ATGL and DGAT while increasing the expression of CEPT1.CONCLUSION:Treatment with SQ can alleviate metabolic dysfunction-associated fatty liver disease(MAFLD)by modulating triglyceride metabolism,phosphatidylcholine metabolism,and dimethylphosphatidylethanolamine lipid me-tabolism,thereby altering the hepatic lipid profile in MAFLD mice.

AIM:This study aimed to investigate the differences in hepatic lipid metabolites in ICR mice in-duced by a high-fat diet and treated with Shaqi concentrated pills(SQ).METHODS:Thirty 8-week-old SPF-grade ICR mice were randomly assigned to five groups:the normal(CON,n=6)group,the high-fat diet model(HFD,n=6)group,the low-dose SQ administration(SQL,n=6)group,the high-dose SQ administration(SQH,n=6)group,and the liver-protecting tablets positive control(PLT,n=6)group.The HFD group was fed a diet consisting of 60%fat for 8 weeks to es-tablish a metabolic-dysfunction-associated fatty liver disease model.Upon successful model establishment,the SQL group received a daily gavage of 395 mg/kg for 4 weeks,while the SQH group received 790 mg·kg-1·d-1.The PLT group was ad-ministered liver-protecting tablets at a dosage of 0.655 g/kg via gavage.Body weight and food intake were monitored week-ly.Liver indices,including Lee's index,triglyceride(TG),total cholesterol(TC),high-density lipoprotein cholesterol(HDL-C),low-density lipoprotein cholesterol(LDL-C),alanine aminotransferase(ALT),and aspartate transaminase(AST)levels,were measured in each group.Hematoxylin-eosin(HE)staining and oil red O staining were performed to assess the extent of pathological damage in liver tissues.Western blot analysis was conducted to evaluate the protein expres-sion levels of choline/ethanolamine phosphotransferase-1(CEPT1),adipose triglyceride lipase(ATGL),and diacylglycerol acyltransferase(DGAT)in the liver.A non-targeted lipidomic analysis using LC-MS was employed to detect changes in hepatic lipid content,and multivariate statistical analyses(principal component analysis and orthogonal partial least squares discriminant analysis)were utilized to compare lipid metabolic profiles among the groups and identify differential lipid metabolites.RESULTS:Compared to the CON group,mice in the HFD group exhibited significantly increased body weight,blood glucose levels,serum TG,TC,LDL-C,ALT,and AST levels,accompanied by a marked decrease in HDL-C levels.HE and oil red O staining results revealed significant lipid droplet accumulation in the liver tissues of HFD mice.In contrast,mice in the SQL and SQH groups showed significant reductions in body weight,blood glucose,serum TG,TC,LDL-C,ALT,and AST levels,along with increased HDL-C levels and less lipid accumulation in liver tissues compared to the HFD group.Staining of liver sections confirmed that SQ treatment mitigated the abnormal accumulation of lipid droplets.Lipidomic analysis indicated that SQ treatment normalized 25 aberrantly expressed lipid metabolites to lev-els comparable to the CON group and identified nine representative differential lipid metabolites.Western blot results dem-onstrated that SQ treatment reduced the protein expression levels of ATGL and DGAT while increasing the expression of CEPT1.CONCLUSION:Treatment with SQ can alleviate metabolic dysfunction-associated fatty liver disease(MAFLD)by modulating triglyceride metabolism,phosphatidylcholine metabolism,and dimethylphosphatidylethanolamine lipid me-tabolism,thereby altering the hepatic lipid profile in MAFLD mice.

Objective To evaluate the role of protein kinase C in the maintenance of chronic inflammatory pain in rats and the relationship with the expression of Nav1.8 in the dorsal root ganglion (DRG).Methods Thirty pathogen-free healthy female Sprague-Dawley rats,weighing 180-220 g,were divided into 3 groups using a random number table:control group (group C),chronic inflammatory pain group (group CIP) and PKC inhibitor group (group P).Normal saline 20 μl was injected into the plantar surface of the right hindpaw every day for 14 consecutive days in group C.Prostaglandin E2 100 ng was injected into the plantar surface of the right hindpaw every day for 13 consecutive days to establish the model of chronic inflammatory pain,and dimethyl sulfoxide 20μl was injected into the plantar surface of the right hindpaw on 14th day in group CIP.Prostaglandin E2 100 ng was injected into the plantar surface of the right hindpaw every day for 13 consecutive days,and PKC inhibitor GF1O9203X 100 nmol/20 μl was injected into the plantar surface of the right hindpaw on 14th day in group P.The mechanical paw withdrawal threshold (MWT) was measured at 1 day before injection (T0) and 1,3,7 and 14 days after the last injection (T1-4).The DRGs of the lumbar segment (L4.5) were removed for determination of Nav1.8 expression using immunofluorescence and Western blot.Results Compared with group C,the MWT was significantly decreased at T1-4 in CIP and P groups,and the expression of Nav1.8 in DRGs was significantly up-regulated in group CIP (P＜0.05).Compared with group CIP,the MWT was significantly increased at T4,and the expression of Nav1.8 in DRGs was down-regulated in group P (P＜0.05).Conclusion Up-regulated expression of Nav1.8 after PKC activation in DRGs is involved in the maintenance of chronic inflammatory pain in rats.