Mechanism of Modified Erchentang on Signaling Pathway of TLR4/MyD88/NF-κB in Lung Tissue of Rats with Chronic Obstructive Pulmonary Disease
10.13422/j.cnki.syfjx.20192203
- VernacularTitle: 二陈汤加味对慢性阻塞性肺疾病大鼠TLR4/MyD88/NF-κB信号通路的影响
- Author:
Li-zhi SHANG
1
;
Shu JI
1
;
Guo-qiang WANG
1
;
Xiao-hui CHEN
1
;
Wen-ying XIE
1
;
Yao-yang LI
1
;
Guang-yuan ZHANG
1
;
Long-tao SHI
1
;
Li-li XU
1
Author Information
1. Henan University of Chinese Medicine, Zhengzhou 450046, China
- Publication Type:Research Article
- Keywords:
chronic obstructive pulmonary disease(COPD);
Erchentang;
Toll-like receptors 4 (TLR4);
nuclear factor-kappa B p65 (NF-κB p65);
monocyte chemoattractantprotein-1 (MCP-1)
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(23):65-72
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To study the effect of modified Erchentang on expressions of Toll-like receptor 4 (TLR4), myeloid differentiation factor (MyD88) and nuclear factor-κB (NF-κB) genes in the lung tissue homogenate of rats with chronic obstructive pulmonary disease (COPD). Method: Forty SD rats were randomly divided into normal group, model group, modified Erchentang group and EVP4593 (NF-κB inhibitor) group. Rat COPD models were prepared through cigarette smoke and tracheal dripping with lipopolysaccharide (LPS). After the modeling, normal and model groups were intragastrically given normal saline solution, EVP4593 group was given EVP4593(1 mg · kg-1) through subcutaneous injection, and modified Erchentang group was given corresponding herbal drugs intragastrically (10 g · kg-1) for 14 days. The levels of high mobility group box 1(HMGB1), chemokines CXCL-2, CXCL-3 and monocyte chemoattractant protein-1 (MCP-1) in rats serum were detected by enzyme-linked immunosorbent assay in rats serum. The expressions of Toll-like receptors 4(TLR4), myeloid differentiation factor (MyD88) and nuclear factor-κB p65 (NF-κB p65) mRNA were detected by Real-time fluorescence quantitative PCR (Real-time PCR) method. Western blot were used to detect the levels of TLR4, MyD88, NF-κB p65 and p-NF-κB p65 protein. Immunohistochemistry (IHC) method was used to detect the localization and expressions of TLR4, MyD88 and p-NF-κB p65 protein in the lung tissue. Result: The mRNA and protein expressions of TLR4, MyD88 and NF-κB p65 were increased significantly (P<0.01) in model group compared with normal group. The levels of HMGB1, CXCL-2, CXCL-3 and MCP-1 in the model group were significantly higher than those in the normal group (P<0.01). Compared with model group, expressions of TLR4, MyD88 and NF-κB p65 mRNA and protein were decreased significantly (P<0.05) in modified Erchentang. Conclusion: Modified Erchentang may inhibit the inflammatory response of COPD effectively. The mechanism may be related to the inhibition of the expressions of the signal molecule genes involved in the TLR4/MyD88/NF-κB pathway and the reduction of the release of HMGB1, CXCL-2, CXCL-3 and MCP-1.
