Xiaoqing Zhuo1,2.#, Wen Gao3,#, Yi Li3, Yanjun Liu3, Xuerui Lun4, Yuqi Cui1*


1Department of Cardiology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, 250021, China - 2Department of Cardiology, Shandong Provincial ENT hospital, Shandong University, Jinan, 250118, China - 3Department of Cardiology, The Fourth People's Hospital of Jinan, Jinan, 250031, China - 4Department of surgical, NO.91951 Military hospital, Qingdao, 266200, China


Background and objective: The relationship of interleukin-10 (IL-10) and angiotensin II receptor 1 (AT1-R) of adjusting the progression of heart failure (HF) is less investigated. The experiment was taken up by surgery with the objective of investigating the mechanism of IL-10 and AT1-R in HF caused. 

Methods: Vehicle, losartan (LOS), LOS along with IL-10, or LOS along with AS101 (an inhibitor of IL-10 biosynthesis) were injected into the mice via paraventricular nucleus (PVN) infusion for 4 weeks. Corticotropin-releasing hormone (CRH), glutamate (Glu), norepinephrine (NE), epinephrine (EPI), tumor necrosis factor-α (TNF-α) fra-like (Fra-LI) and gamma-aminobutyric acid (GABA) activity were determined by ELISA, Western blot and immunohistochemistry.

Results: CRH, Glu, NE, EPI, TNF-α and Fra-LI were higher, while lower level of GABA in HF group compared to those in Sham group. The treatment of LOS and/or IL-10 can attenuat the decrease in GABA, with the increase in CRH, Glu, NE, EPI and TNF-α. And it makes no difference of expression in CRH, Glu, NE, EPI, TNF-α and GABA levels between LOS group and LOS+IL-10 group. But there were higher levels of cell factors foregoing except lower level of GABA in HF mice treated with LOS+AS101, and Fra-LI-positive in PVN neurons, than mice treated with LOS or LOS+IL-10.

Conclusion: These results of this study demonstrate that there has an interactivity between AT1-R and IL-10 in the deterioration of HF. 


heart failure, paraventricular nucleus, interkin-10, inflammation, angiotensin.