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Background Cigarette smoke induces persistent pulmonary inflammation and oxidative stress. Shenling Baizhu San (SLBZS) has shown anti-inflammatory activity, but its complex composition limits standardization. This study evaluated a SLBZS-derived defined-component formula (DCF) in rats during ongoing cigarette smoke exposure. Methods Seventy male Sprague-Dawley rats were randomly assigned to seven groups (n = 10/group): control, model, dexamethasone, commercial SLBZS, and low-, medium-, and high-dose DCF groups. DCF was administered at approximately 2.75, 5.49, and 10.98 mg/kg/day, respectively. Except for controls, rats underwent cigarette smoke exposure for 120 min/day for 8 weeks, with drug administration initiated concurrently. Lung tissue levels of IL-1 β , IL-6, TNF- α , CXCL1, CCL2, 8-iso-PGF2 α , MDA, and SOD were measured. Lung histopathology and p-p38 and p-p53 protein levels were also assessed. Results Cigarette smoke exposure increased IL-1 β , IL-6, TNF-α, CXCL1, CCL2, and 8-iso-PGF2 α levels, reduced SOD activity, and increased p-p38 and p-p53 protein levels compared with controls ( $$p < 0.05$$ ). Medium- and high-dose DCF reduced these inflammatory and oxidative injury-related changes and improved histopathological abnormalities ( $$p < 0.05$$ ). MDA levels did not differ significantly among groups. Conclusion Concurrent DCF administration attenuated cigarette smoke-induced lung inflammation and oxidative injury during continued smoke exposure. The accompanying reductions in p-p38 and p-p53 suggest possible involvement of related stress-response pathways, although causal pathway regulation was not established.
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Liu et al. (2026) studied this question.
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