[ Formula alleviates chronic obstructive pulmonary disease in rats with pulmonary deficiency syndrome by regulating NLRP3/GSDMD pyroptosis pathway].

OBJECTIVE

To investigate the effects of (SQWF) Formula on the NLRP3/GSDMD signaling pathway in pulmonary deficiency syndrome rats with chronic obstructive pulmonary diseases (COPD).

METHODS

Rat models of COPD and lung deficiency syndrome induced by exposure to cigarette smoke and lipopolysaccharide (LPS) injection were randomized (=8) for treatment with low-, medium- and high-dose SQWF or (YPF). The changes in body weight, grip strength, lung function, pulmonary pathology, peripheral blood inflammatory cell counts, and levels of inflammatory factors in the bronchoalveolar lavage fluid (BALF) were examined. The expressions of proteins associated with the NLRP3/GSDMD signaling pathway in the lung tissues were determined with RT-qPCR and immunohistochemistry.

RESULTS

The rat models of COPD and lung deficiency syndrome showed significantly reduced body weight, grip strength and lung function (<0.01) with severe lung pathologies, increased levels of WBC, NEU% and MON% (<0.01), decreased LYM% (<0.01), and increased levels of TNF-α, IL-6, IL-1β and IL-18 in the BALF (<0.01); the mRNA and protein expression levels of NLRP3, ASC, GSDMD and IL-1β all increased significantly in the lung tissue (<0.01). Treatment with SQWF and YPF obviously increased body weight and improved grip strength, pulmonary function and lung pathology of the COPD rats (<0.05). The treatments obviously improved the changes in peripheral blood inflammatory cell counts and inflammatory factors in the BALF of the rat models (<0.01) and lowered the expressions of NLRP3, ASC, GSDMD and IL-1β in the lung tissues (<0.05) without significantly affecting the mRNA levels of caspase-1 and IL-18 (>0.05), and the effects of SQWF were dose-dependent.

CONCLUSION

SQWF Formula relieves inflammatory response and injury in the lung tissue of COPD rats with pulmonary qi deficiency syndrome possibly by inhibiting pyroptosis through regulating the NLRP3/GSDMD pathway.