Sodium Ferulate Protects against Angiotensin II-Induced Cardiac Hypertrophy in Mice by Regulating the MAPK/ERK and JNK Pathways.
Background and Objective. It has been reported that sodium ferulate (SF) has hematopoietic function against anemia and immune regulation, inflammatory reaction inhibition, inhibition of tumor cell proliferation, cardiovascular and cerebrovascular protection, and other functions. Thus, this study aimed to investigate the effects of SF on angiotensin II- (AngII-) induced cardiac hypertrophy in mice through the MAPK/ERK and JNK signaling pathways.Methods. Seventy-two male C57BL/6J mice were selected and divided into 6 groups: control group, PBS group, model group (AngII), model + low-dose SF group (AngII + 10 mg/kg SF), model + high-dose SF group (AngII + 40 mg/kg SF), and model + high-dose SF + agonist group (AngII + 40 mg/kg SCU + 10 mg/kg TBHQ). After 7 d/14 d/28 days of treatments, the changes of blood pressure and heart rates of mice were compared. The morphology of myocardial tissue and the apoptosis rate of myocardial cells were observed. The mRNA and protein expressions of atrial natriuretic peptide (ANP), transforming growth factor-β(TGF-β), collagen III (Col III), and MAPK/ERK and JNK pathway-related proteins were detected after 28 days of treatments.Results. SF improved the mice's cardiac abnormality and decreased the apoptosis rate of myocardial cells in a time- and dose-dependent manner (allP< 0.05). MAPK/ERK pathway activator inhibited the protective effect of SF in myocardial tissue of mice (P< 0.05). SF could inhibit the expression of p-ERK, p-p38MAPK, and p-JNK and regulate the expressions of ANP, TGF-β, and Col III (allP< 0.05).Conclusion. Our findings provide evidence that SF could protect against AngII-induced cardiac hypertrophy in mice by downregulating the MAPK/ERK and JNK pathways.
Emergency Department, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.
Bo
B
Hu
Emergency Department, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.
Jian-Tao
JT
Song
Emergency Department, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.
Xian-Fei
XF
Ji
Emergency Department, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.
Zun-Qi
ZQ
Liu
Emergency Department, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.
Mu-Lin
ML
Cong
Emergency Department, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.
Dong-Xing
0000-0003-4219-4897
DX
Liu
D000804:Angiotensin II; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D006332:Cardiomegaly / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000201:enzymology* / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D003373:Coumaric Acids / Q000494:pharmacology / Q000627:therapeutic use*; D003971:Diastole / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D006339:Heart Rate / Q000187:drug effects; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013599:Systole / Q000187:drug effects
D002316:Cardiotonic Agents; D003373:Coumaric Acids; D012333:RNA, Messenger; D000804:Angiotensin II; C004999:ferulic acid; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases