Effects of panax notoginseng saponin on the pathological ultrastructure and serum IL‐6 and IL‐8 in pulmonary fibrosis in rabbits

三七 乳酸脱氢酶 肺纤维化 医学 免疫印迹 羟脯氨酸 药理学 肌酸 白细胞介素 纤维化 病理 内科学 免疫学 化学 生物化学 细胞因子 替代医学 基因
作者
Zhang Ji-zhou,Qing Li,Qiqi Shao,Jingling Song,Bin Zhou,Peng Shu
出处
期刊:Journal of Cellular Biochemistry [Wiley]
卷期号:119 (10): 8410-8418 被引量:20
标识
DOI:10.1002/jcb.27045
摘要

Panax notoginseng saponin (PNS) constitutes the major effective components of Panax notoginseng, which is widely used to treat microcirculatory disturbance associated diseases. In this study, we designed to investigate the effect of PNS on the treatment of pulmonary fibrosis (PF) and further explored its mechanism. A total of 40 healthy Japanese White rabbits were randomly divided into five groups (control group; PF model group; PNS prevention group; PNS treatment group; and western medicine [prednisone acetate] treatment group). Expression of hydroxyproline (HYP), fibronectin (FN), aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), interleukin-6 (IL-6), and interleukin-8 (IL-8) in serum was detected using corresponding detection kits. Western blot was applied to detect the expression of p50 and p65 in pulmonary tissues. The pathological variations of the cardiac and pulmonary ultrastructure were observed under both the optical and electron microscope. PF models were established successfully. The results showed that compared with the other groups, PNS groups (PNS prevention and treatment group) apparently relieved the cardiopulmonary injury, and reduced IL-6 and IL-8 expression levels in the serum. Furthermore, the PNS groups performed better in relieving cardiopulmonary injurythan other groups. Both the PNS groups and the western medicine treatment group presented an obvious role in relieving PF. We concluded that PNS could reduce the expression of AST, LDH, CK, IL-6, and IL-8 in serum of the rabbits, relieve the pathological ultrastructure of cardiopulmonary injury, alleviate PF. And it might be attributed to the inhibition on the NF-κB signaling pathway.

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