Treatise·QIUZHEN
LIANG Yingjin, ZHANG Kang, JIA Mingyan, JING Pengzhen, XIE Kai, WANG Haifeng
China Journal of Traditional Chinese Medicine and Pharmacy.
2025, 40(5):
2579-2586.
Objective: To investigate whether Qingfei Jiedu Huatan Formula (QJHF) can improve lung and intestinal damage in severe pneumonia (SP) rats by inhibiting the activation of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome. Methods: A total of 180 SPF rats were divided into five groups: Control, Model, QJHF, QJHF+MCC950, and Moxifloxacin. A SP rat model was established via tracheal intubation and instillation of Klebsiella pneumoniae solution. MCC950 was administered intraperitoneally to the rats one hour before model induction. The QJHF and QJHF+MCC950 groups received QJHF, while the Moxifloxacin group received Moxifloxacin. All treatments were administered orally for one week. To evaluate lung tissue inflammatory injury, we measured arterial blood oxygen tension (PaO2), PaO2/FiO2, examined lung morphology, and performed HE staining. Claudin-4, ZO-1, Occludin1, NLRP3, ASC, and Caspase-1 (p10) proteins in intestinal tissues were detected by Western Blot. NLRP3, ASC, Caspase-1 (p10), IL-18 and IL-1β in lung tissues were assessed by immunohistochemical staining. IL-18 and IL-1β in intestinal tissues were measured by ELISA. Results: Compared to the Control group, the arterial PaO2 and PaO2/FiO2 of rats in the Model group were significantly decreased (P<0.01), pulmonary consolidation and inflammatory infiltration increased, lung injury scores significantly rose (P<0.01), and the expression of Claudin-4, ZO-1 and Occludin-1 proteins in intestinal tissues markedly decreased (P<0.01), in contrast, the expression of NLRP3, ASC, Caspase-1 (p10), IL-18, and IL-1β in lung and intestinal tissues significantly increased (P<0.01). Compared to the Model group, on the 4th and 7th days of treatment in each medication group, PaO2 and PaO2/FiO2 significantly increased (P<0.01, P<0.05), pulmonary inflammatory infiltration improved, lung injury scores significantly decreased (P<0.01), the expression of Claudin-4, ZO-1 and Occludin-1 proteins in intestinal tissues significantly increased (P<0.01, P<0.05), and the expression of NLRP3, ASC, Caspase-1 (p10), IL-18, and IL-1β significantly decreased (P<0.01, P<0.05). Conclusion: QJHF can effectively treat SP, which is associated with the inhibition of NLRP3 inflammasome activation, the reduction of inflammatory responses in lung and intestinal tissues, and the improvement of intestinal mucosal barrier function.