Baicalin inhibits inflammation in rats with chronic obstructive pulmonary disease. - GreenMedInfo Summary
Baicalin Inhibits Inflammation in Rats with Chronic Obstructive Pulmonary Disease by the TLR2/MYD88/NF-Bp65 Signaling Pathway.
Evid Based Complement Alternat Med. 2022 ;2022:7273387. Epub 2022 Jul 22. PMID: 35911168
Jiangang Ju
Objective: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease with a relatively high morbidity and death rate. This study aimed to investigate the inhibitory effect of baicalin (BA) on inflammation in COPD rats and its possible mechanism.
Methods: The experimental COPD of SD rats were induced by LPS, smoking, and cold stimulation, and they were randomly divided into the control group, COPD group, COPD + LB group, COPD + MB group, and COPD + HB group. The test of pulmonary function and the HE staining were carried out in COPD rats. The levels of TNF-, IL-1, IL-6, IL-10, and IL-8, as well as GSH, SOD, and MDA in serum, were detected by ELISA. The levels of TLR2, MYD88, TNF-and IL-1mRNA in BALF were detected by qPCR. The expression of TLR2/MYD88/NF-Bp65 pathway-related proteins was also detected by the Western blot and immunohistochemistry assays.
Results: Compared to the COPD model group, BA treatment significantly improved the pulmonary function and pathologic changes, reduced the levels of TNF-, IL-1, IL-6, IL-10, IL-8, and MDA, and increased the levels of IL-10, SOD, and GSH in COPD rats. In addition, BA could also decrease the protein levels of MYD88, p-NF-Bp65/NF-Bp65, TLR2, and TLR4 but increase the protein level of p-IBa/IB in lung tissue of COPD rats.
Conclusion: BA ameliorated inflammatory response and oxidative stress in COPD rats by regulating the TLR2/MYD88/NF-Bp65 signaling pathway.