Changes of Leptin and Janus Protein Tyrosine Kinase 2/Activating Transcriptor 3 Signal Transduction Pathways in Experimental Rats of Heart Failure With Cachexia / 中国循环杂志

ABSTRACT

Objective: To investigate the changes of serum levels of leptin in chronic heart failure (CHF) rats with cachexia and to study its mechanism via leptin receptor expression and leptin signal transduction pathways. Methods: There were 15/60 male SD rats were randomly used as Control group. CHF model was established in rest 45 rats by isoproterenol hydrochloride (ISO) injection as CHF group, n=36;9 rats died. According to body weight changes and echocardiography examination, CHF rats were further divided into 2 groupscCHF group, the rats with cachexia, n=16 and ncCHF group, the rats with non-cachexia, n=20. Serum levels of leptin and protein levels of janus activating kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), suppressor of cytokine signaling 3 (SOCS3) were examined by ELISA;the expressions of leptin receptor in the myocardial and adipose tissues were observed by immunohistochemistry;mRNA expressions of JAK2, STAT3 and SOCS3 in adipose tissue were detected by RT-PCR. Results: Serum levels of leptin, JAK2, STAT3 and the expressions of JAK2, STAT3 in adipose tissue were higher in both ncCHF and cCHF groups than Control group, P0.05. Serum levels of leptin, SOCS3 and mRNA expression of SOCS3 in cCHF group were lower than ncCHF group, P Conclusions: Increased serum level of leptin was involved in HF occurrence, leptin receptor expression and JAK2/STAT3 signal transduction pathways might be related to CHF combining cachexia in experimental rats.