ABSTRACT
Objective To explore the effect of FGF21 on MSG-induced nonalcoholic fatty liver diseases of inflammation and TLR4/p38MAPK signal pathway in rats.Methods Newborn SD rats were randomly divided into control group,MSG group and FGF21 group(n =10).Rats of MSG group and FGF21 group were adiministered with solution of MSG 4g/(kg · d) at 2nd,4th,6th,8th and 10th postnataldays.After being fed for thirteen weeks,rats of FGF21 group was intraperitoneal injected with FGF21 1 mg/(kg · d) for a continuous 32 days.Liver pathology of the rats was analyzed by HE staining.The liver weight,aminotrasferases were observed.The expression of IL-6,TNF-α,TLR4,p38MAPK in liver tissue were determined by fluorescence quantitative PCR and Western blot.Results Compared with the control group,liver tissues of the MSG group changed to bullous steatosis and had inflammatory cell infiltration,the liver weighted,serum activities of ALT,AST,ALP were increased (P ＜ 0.01,P ＜ 0.01,P ＜ 0.01,P ＜ 0.01).The expression of IL-6,TNF-α,TLR4,p38MAPK mRNA and protein expression of TLR4,p38MPAK,p-p38MAPK in rats hepatocyte were increased than those in control group (P ＜ 0.01).After reatment with FGF21,the bullous steatosis and inflammatory cell,liver weighted,serum activities of ALT,AST,ALP were signficantly decreased (P ＜ 0.05,P ＜ 0.01,P ＜ 0.01,P ＜ 0.05),and the levels of IL-6,TNF-a,TLR4,p38 MAPK mRNA and protein expression of TLR4,p38-MPAK,p-p38MAPK were reduced than those of MSG group(P ＜0.01).Conculsion The FGF21 may regulate MSG-induced NAFLD of inflammation through TLR4/p38MAPK signaling pathway in rats.
ABSTRACT
Objective To investigate the protective effect and possible mechanism of Gossypol on isolated myocardial ischemia/reperfusion injury in rats.Methods 40 male Sprague-Dawley rats were randomly divided into 4 groups:Blank group,heart ischemia reperfusion group (MI/R group),high and low-dose Gossypol group (40,20 mg/L).The model of the myocardial ischemia/reperfusion injury were established using the Langendorff method.The hemodynamicsindexes,cardiac enzymes AST and LDH,inflammatory cytokines (NF-κB,ICAM-1,TNF-α and IL-6) were measured.The effect and mechanism of Gossypol on early-stage MI/R of the oxidative stress response and the JNK/p38 MAPK signal pathway were investigated.Results Experimental results showed that Gossypol could significantly improve the functional capacity of the heart,reduce the contents of AST,LDH and inflammatory cytokines in reperfused heart tissue,and increase superoxide dismutase levels to protect the heart.The mechanism of this substance may involve anti-lipid peroxidation and inhibition of p38 kinase phosphorylation and JNK,and reduction of oxidative stress injury and apoptosis damage induced by MI/R.Conclusion This study confirm that Gossypol exerts extensive anti-MI/R effects.Its mechanism may be related to the interfering with the oxidative stress response and suppressing the JNK/p38 MAPK signal pathway.
ABSTRACT
Objective:To investigate the inhibitory effect of 4'-methylether-scutellarein(4-MS),an extract from Verbena officinalis,on human choriocarcinoma JAR cell line and the possible mechanism.Methods:JAR cells were exposed to 4'-methylether-scutellarein of different concentrations for 48 h.MTT assay was used to examine the anti-proliferative effect of 4'-methylether-scutellarein.Flow cytometry was used to investigate the apoptosis and the changes of cell cycle.AO/EB double staining was applied to discriminate the apoptotic cells from dead ones.The changes of Survivin,p38-MAPK and Caspase 3 mRNA expressions were detected by RT-PCR in JAR cells treated with 4-MS.Furthermore,Western blotting assay was used to determine Survivin protein expression,phosphorylation level of p38 and Caspase 3 in JAR cells before and after 4-MS treatment.Results:4-MS inhibited the proliferation of JAR cells in a dose- and time-dependent manner(P