Impacts of Phenylephrine on Myocardial Fibrosis Regulation and Interleukin-1, Interleukin-6, Tumor Necrosis Factor-α Expressions in Experimental Mice
10.3969/j.issn.1000-3614.2016.03.020
- VernacularTitle:苯肾上腺素对心肌纤维化的调节和对白细胞介素-1、白细胞介素-6及肿瘤坏死因子-α的影响
- Author:
Shuo WANG
;
Xiao PANG
;
Hui CAO
- Publication Type:Journal Article
- Keywords:
Adrenergic alpha-1 receptor agonists;
Myocardial ifbrosis;
Interleukin-1;
Interleukin-6;
Tumor necrosis factor-α
- From:
Chinese Circulation Journal
2016;31(3):289-293
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explicit phenylephrine (PE), α1-adrenergic receptor (α1-AR) on myocardial fibrosis regulation and interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α) expressions in pressure overloaded mice.
Methods:A total of 49 KM mice were randomly divided into 3 groups: Blank control group, n=7, Sham operation group, n=7, Transverse abdominal aortic constriction (TAC) group, n=35, and 8 weeks later, the mice in TAC group were further divided into 5 sub-groups as TAC control, TAC+PE, TAC+Praz, TAC+Prop, TAC+Carv sub-groups, n=5 in each sub-group, and the animals were respectively treated for 3 weeks. Left ventricular collagen volume fraction (CVE), hydroxyproline content and IL-1, IL-6, TNF-α expressions were examined respectively.
Results: By 8 weeks treatment, compared with Blank control group, TAC group had obvious myocardial fibrosis, increased hydroxyproline content and IL-1, IL-6, TNF-α expressions,P<0.001. Compared with TAC control sub-group, TAC+PE, AC+Prop, TAC+Carv sub-groups showed decreased CVF, hydroxyproline content and IL-1, IL-6, TNF-αexpressions,P<0.001, while the above changes were not obvious in TAC+Praz sub-group,P>0.05; CVE and hydroxyproline content were similar between TAC+PE and TAC+Prop sub-groups, while the expressions of IL-1, IL-6 and TNF-α were obviously decreased in TAC+Prop sub-group,P<0.05. Conclusion: PE may improve myocardial ifbrosis and IL-1, IL-6, TNF-α expressions by activating α1-AR in pressure overloaded mice, α1-AR might be a defending factor for myocardial ifbrosis.
