Protective effects of Isodon Suzhouensis extract and glaucocalyxin A on chronic obstructive pulmonary disease through SOCS3–JAKs/STATs pathway

Abstract

Chronic obstructive pulmonary disease (COPD) is an irreversible disease with the leading causes of morbidity, mortality, and several physical limitations. Isodon Suzhouensis is a unique Chinese medicinal plant used for both medicine and food. It possesses strong anti‐inflammatory effects that may treat COPD. Considering the fact that the effects of Isodon Suzhouensis extract (WZZE) and its active ingredient glaucocalyxin A (GLA) on COPD have never been reported before, this study aimed to investigate the effects of WZZE and GLA against COPD and its underlying mechanistic pathway in COPD model rats or in CSE‐induced NR8383 cells. The variation in lung physiology was measured through spirometry while histopathological changes were studied via H&E staining of the COPD model rats lung samples. The levels of cytokine and other immunomodulatory proteins were determined by ELISA. Apoptosis of lung tissue cells was detected by TUNEL staining. Western blot and immunohistochemistry were used to detect the expression of related pathways and other proteins. The results show that WZZE improved the relevant lung function indicators, while restoring the activity of immunoglobulins (Ig A, IgG) and inhibiting the levels of TNF‐α and IL‐1β in serum and bronchoalveolar lavage fluid, thereby improving the body's immunity and inhibiting inflammation of the airways and lungs, slowing the progression of COPD. The results of H&E staining indicated that WZZE is capable of improving the pathological injury associated with COPD. In addition, the administration of WZZE reduced the expression of MUC5AC protein induced and the apoptosis rate of lung tissue cells in COPD model rats. The results also showed that WZZE significantly increased the expression of SOCS3 and inhibited the expression of JAKs/STATs pathway‐related proteins in COPD rats. In addition, GLA can also upregulate the expression of SOCS3 protein, inhibit JAKs/STATs pathway, inhibit the expression level of MUC5AC, upregulate the expression level of immunoglobulin, and downregulate the expression level of proinflammatory factors in NR8383 cells induced by CSE. Present study findings suggest that WZZE and GLA may ameliorate the progression of COPD via the SOCS3–JAKs/STATs pathway in COPD rats or in CSE‐induced NR8383.

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