Chronic obstructive pulmonary disease (COPD) is a serious chronic lung disease. Schisandrin A (SchA) is one of the most important active ingredients inSchisandra chinensisand has been used to treat various lung diseases in several countries. Here, we studied the pharmacological effect of SchA on airway inflammation induced by cigarette smoke (CS) and explored the therapeutic mechanism of SchA in COPD model mice. Our results showed that SchA treatment significantly improved the lung function of CS-induced COPD model mice and reduced the recruitment of leukocytes and hypersecretion of interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in bronchoalveolar lavage fluid (BALF). H&E staining showed that SchA treatment could effectively reduce emphysema, immune cell infiltration and airway wall destruction. In addition, we found that SchA treatment can stimulate the expression of heme oxygenase-1 (HO-1) through the nuclear factor-erythroid 2-related factor (Nrf2) pathway, significantly reduce oxidative stress, increase catalase (CAT) and superoxide dismutase (SOD) levels, and suppress the level of malondialdehyde (MDA) in COPD model mice. Moreover, SchA treatment suppressed the generation of the NLRP3/ASC/Caspase1 inflammasome complex to inhibit the inflammatory response caused by IL-1β and IL-18 and pyroptosis caused by GSDMD. In conclusion, our study shows that SchA treatment can inhibit the production of ROS and the activation of the NLRP3 inflammasome by upregulating Nrf-2, thereby producing anti-inflammatory effects and reducing lung injury in COPD model mice. More importantly, SchA exhibited similar anti-inflammatory effects to dexamethasone in COPD model mice, and we did not observe substantial side effects of SchA treatment. The high safety of SchA makes it a potential candidate drug for the treatment of COPD.

Background: The previous studies reported the antioxidant and anti-inflammatory properties of Schisandrin A (Sch A). This study aimed to investigate the ability of Sch A to protect against lung oxidative stress induced by the combination of cigarette smoke extract and lipopolysaccharide (LPS) in an in vitro model of chronic obstructive pulmonary disease (COPD). Methods: The cell viability was determined by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Colorimetry was used to detect the changes in antioxidant markers. Quantitative real-time polymerase chain reaction (RT-PCR) was used to examine the mRNA levels of interleukin-8 (IL-8) and heme oxygenase-1 (HO-1). The levels of IL-8 and HO-1 in the supernatant were determined by enzyme-linked immunosorbent assay, and Western blot analysis was performed to measure the phosphorylation and protein expression levels of nuclear factor-κB. Results: Sch A inhibited the excessive proliferation of pulmonary epithelial cells, decreased malondialdehyde content, and increased the expression levels of superoxide dismutase and glutathione after the combined treatment of cigarette smoke extract and LPS. Also, Sch A downregulated the expression of IL-8 and upregulated the expression of HO-1 mRNA in lung epithelial cells and cell supernatants, and resulted in the downregulation of the protein expression level of phosphorylated nuclear factor-κB. Conclusions: Sch A inhibited the oxidative stress of lung epithelial cells induced by the combination of cigarette smoke extract and LPS. Sch A may be a potential therapeutic medication for COPD.

Does Chronic Kidney Disease Result in High Risk of Atrial Fibrillation?

Objective: Quanzhen Yiqi decoction (QZYQ) is a traditional Chinese medicine for treating chronic obstructive pulmonary disease. Methods: Mice were exposed to cigarette smoke (CS) 6 days/week (40 cigarettes/day) for 24 weeks and then intragastrically administered QZYQ (4.72, 9.45, or 18.89 g/kg) or dexamethasone (DEX, 0.6 mg/kg) for 6 weeks. We examined the lung function and collected bronchoalveolar lavage fluid for inflammatory cell and cytokine quantification. The pathological lung changes, ROS and oxidative biomarkers were measured. We used immunohistochemistry and western blotting to evaluate the levels of Nrf2/HO-1, NLRP3/ASC/Caspase1/IL-1β/IL-18. Results: The CS group showed significant increases in the forced vital capacity, lung resistance, and chord compliance and a lower FEV50/FVC compared with the control, and QZYQ improved these changes. In addition, QZYQ effectively reduced emphysema, immune cell infiltration, and airway remodeling. QZYQ stimulated HO-1 expression and reduced oxidative stress through the Nrf2 pathway. QZYQ inhibited the production of NLRP3/ASC/Caspase-1 to inhibit IL-1β and IL-18. Conclusion: Our study suggested that QZYQ can improve the function and histology of the lungs and reduce inflammatory cell recruitment. QZYQ inhibits ROS production and NLRP3 inflammasome activation by upregulating Nrf2 to reduce lung injury. The anti-inflammatory effects of QZYQ are similar to those of DEX.