Objective To investigate the influence of Qingre Huatan Jiedu prescription on lung tissues of rats with apoplexy?associated pneumonia, and its relationships with the Akt/ c?Jun amino terminal kinase 3 (JNK3) / caspase?3 and nuclear factor κB (NF?κB) signaling pathway. Methods SD rats were divided into a sham group, model group (cerebral ischemia reperfusion lung injury rats), Qingre Huatan Jiedu prescription low?dose group (7 mg/ kg), intermediate?dose group (14 mg/ kg), high?dose group (28 mg/ kg), and nimodipine group (200 mg/ kg), with 24 rats in each group. Pathological changes of lung tissues in rats were observed by the naked eye and hematoxylin?eosin staining (HE). The wet weight and dry weight of lung tissues and arterial oxygen partial pressure in rats were also measured, enzyme?linked immunosorbent assay was used to determine the oxidative index level in lung tissue, while western blot and immunohistochemistry were used to detect Akt, p?Akt, JNK3, p?JNK3, Caspase?3, p65, and p50 expression. Results Compared with those in the sham group, W/ D, PMN, MDA, TNF?α, IL?1β, lung tissue classification, lung tissue pathological score, the expression of p?JNK3, Caspase?3, p65, and P50 protein, and the positive expression rates of p?JNK3, p65, and P50 protein of lung tissue in the model group were all increased, while PaO2 , OI, SOD, the expression of p?Akt protein, and positive protein expression in lung tissue were all decreased. Compared with those in the model group, W/ D, PMN, MDA, TNF?α, IL?1β, lung tissue classification, lung tissue pathological score, the expression of p?JNK3, Caspase?3, p65, and P50 protein, and the positive expression rates of p?JNK3, p65, and P50 protein of lung tissue in the positive group and the Qingre Huatan Jiedu prescription group were all decreased, while PaO2 , OI, SOD, the expression of p?Akt protein, and positive protein expression in lung tissue were all decreased, in a dose?dependent manner ( P <0. 05). Conclusions Qingre Huatan Jiedu prescription has a certain protective effect against lung injury in rats with apoplexy?associated pneumonia. Its mechanism of action may be related to inhibition of the JNK3/ Caspase?3 and NF?κB signaling pathway and activation of Akt expression.