Baicalin Inhibits Inflammation in Rats with Chronic Obstructive Pulmonary Disease by the TLR2/MYD88/NF-κBp65 Signaling Pathway

Abstract

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-α, IL-1β, 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-α, and IL-1β mRNA in BALF were detected by qPCR. The expression of TLR2/MYD88/NF-κBp65 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-α, IL-1β, 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–κBp65/NF-κBp65, TLR2, and TLR4 but increase the protein level of p-IκBa/IκB in lung tissue of COPD rats. Conclusion. BA ameliorated inflammatory response and oxidative stress in COPD rats by regulating the TLR2/MYD88/NF-κBp65 signaling pathway.

Suppressing inflammatory signals and apoptosis-linked sphingolipid metabolism underlies therapeutic potential of Qing-Jin-Hua-Tan decoction against chronic obstructive pulmonary disease

“…Mechanistically, acacetin could bind MEK1/2, ERK1/2, Bcl2, NF-κB, and alCDase according to the results of our docking analysis, which elucidates the signaling modulation by QJHTD and indirectly testifies to the role of acacetin as an effective compound in this preparation. However, molecular docking exhibited low affinity between baicalin and target proteins, indicating that baicalin may exert its action on COPD via distinct signaling cascades, as previously reported [ [42] , [43] , [44] ]. Overall, acacetin and baicalin may act synergistically via complementary molecular routes to assist in the anti -COPD properties of QJHTD.…”

Pharmacological effects of baicalin in lung diseases

“… Hao et al (2021) demonstrated that baicalin upregulated the expression of heat shock protein 72 (HSP72), resulting in the inhibition of c-Jun N-terminal kinase (JNK) signaling activation and ultimately relieving COPD. Recently, Ju et al (2022) proved that baicalin controlled the TLR2/myeloid differentiation primary response gene 88 (MYD88)/NF-κB p65 signaling pathway to reduce oxidative stress and the inflammatory response in COPD rats. Through regulating oropharyngeal microbiota and influencing the expression of the High Mobility Group Protein 1 (HMGB1)/Caspase1 pathway, baicalin may also mitigate mouse lung inflammatory injury caused by exposure to PM2.5 ( Deng et al, 2022 ).…”

An Update on Toll-like Receptor 2, Its Function and Dimerization in Pro- and Anti-Inflammatory Processes

“…A study from 2021 showed that a high number and blockwise distribution of certain methyl esters of pectins were responsible for a TLR2/1-dependent anti-inflammatory effect [87]. Interestingly, the flavonoid baicalin isolated from Scutellaria baicalensis Georgi inhibited inflammation in rats with chronic obstructive pulmonary disease via the TLR2/MyD88/NF-κB pathway [88]. Furthermore, the anti-inflammatory properties of TLR2 were evident in response to polysaccharide A (PSA) from Bacteroides fragilis in B cells and T cells, resulting in the production of IL-10 and interferon-γ (IFN-γ) [89][90][91].…”