Baicalin attenuates inflammation by inhibiting NF-κB activation in cigarette smoke induced inflammatory models

Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a key player in the inflammatory response. Baicalin is an extract from roots of the plant scutellaria baicalensis. Many studies show that baicalin has anti-inflammatory, anti-bacterial and antiviral activities. Here we investigated the influence of baicalin on COPD inflammation and the mechanism of anti-inflammatory effect in vivo and in vitro. In vivo, COPD rat model was established by cigarette smoke (CS) exposure. Thirty-six Sprague–Dawley (SD) rats were randomly assigned to six experimental groups: control, CS, dexamethasone (DXM), and baicalin (20 mg/kg, 40 mg/kg, 80 mg/kg). The lung pathology was observed and leukocytes in bronchoalveolar lavage fluid (BALF) were counted by Optical microscope. Pulmonary function was measured by using an animal plethysmograph. The production of cytokines was measured by ELISA and the expression levels of NF-κB p65 protein were detected by immunohistochemistry. The results in vivo show CS exposure significantly increased the expression of IL-8, IL-6 and TNF-α in plasma and BALF and enhanced NF-κB p65 expression in the lungs. Baicalin treatment markedly attenuated the inflammatory effects of CS. In vitro, cell model was established by using cigarette smoke extract (CSE) to stimulate type II pneumocytes. Type II pneumocytes were also divided into six groups: control, CSE, pyrrolidine dithiocarbamate (PDTC), and baicalin (5 μmol, 10 μmol, 20 μmol). Cytokines levels were measured by ELISA. Expression of IκB and p65 phosphorylation was detected by western blotting. NF-κB DNA-binding activity was detected by EMSA. The results show that CSE resulted in increasing IL-8, IL-6 and TNF-α expression and activation of NF-κB. The proinflammatory effects of CSE were inhibited by treatment of baicalin in a dose-dependent manner. It can be concluded that baicalin has significant anti-inflammatory effects on CS induced COPD rat models and CSE-induced cell models, and the effectiveness increases with increasing baicalin dosage. The anti-inflammatory effect is likely achieved by inhibiting the NF-κB pathway.