Abstract
Abstract
Background:
Cigarette smoke exposure is a major cause of chronic airway inflammation. Although smoking cessation remains the cornerstone intervention, established inflammatory and epithelial alterations may persist in some individuals. Shenling Baizhu San (SLBZS), a multi-component herbal formula, has demonstrated anti-inflammatory potential in experimental studies, but its complex composition limits standardization and mechanistic interpretation. This study evaluated the effects of a SLBZS-derived defined-component formula on cigarette smoke-induced airway inflammation in rats and preliminarily explored its association with p-p38/p-p53-related responses.
Methods:
Seventy 8-week-old male Sprague-Dawley rats weighing 220--250 g were randomly divided into seven groups (n = 10 per group): control, model, positive control (dexamethasone, 0.5 mg/kg/48 h, intraperitoneal injection), commercial SLBZS preparation (10 mL/kg/day, gavage), and low-, medium-, and high-dose defined-component formula groups (total mixture doses of approximately 3.29, 6.58, and 13.16 mg/kg/day, respectively, by gavage). The defined-component formula consisted of seven purified compounds: ginsenoside Rb1, atractylenolide III, pachymic acid, platycodin D, batatasin III, glycyrrhizic acid, and liquiritigenin. Except for the control group, rats were exposed to cigarette smoke for 120 min daily for 8 consecutive weeks. Levels of inflammatory cytokines and chemokines, including IL-1$\beta$, IL-6, TNF-$\alpha$, CXCL1, and CCL2, as well as oxidative stress-related indicators, including 8-iso-PGF2$\alpha$, MDA, and SOD activity, were measured in lung tissue homogenates using commercial assay kits. p-p38 and p-p53 protein levels in lung tissue were detected by Western blot, and lung histopathology was examined by hematoxylin and eosin staining.
Results:
Compared with the control group, the model group showed increased levels of IL-1$\beta$, IL-6, TNF-$\alpha$, CXCL1, CCL2, and 8-iso-PGF2$\alpha$ in lung tissue homogenates, decreased SOD activity, and increased p-p38 and p-p53 protein levels in lung tissue (P $Conclusion:
The SLBZS-derived defined-component formula attenuated cigarette smoke-induced airway inflammation in rats, as evidenced by reduced inflammatory cytokine and chemokine levels, improved lung histopathology, and restored SOD activity. The decrease in p-p38 and p-p53 levels suggests that a p-p38/p-p53-related mechanism may be involved. Because pathway-specific interventions were not performed, the mechanistic conclusion should be interpreted as exploratory.