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| Study on the protective effect and mechanism of Tibetan Medicine Ershiwuwei Feibing Pills on acute lung injury in rats |
| LI Yaxuan1 LI Weihong1 REN Qingjia2 YE Fei1 GUO Haolin1 LI Tenghui1 FAN Angran1 DU Qinghong1 |
1.School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China;
2.Graduate School, Tibet Medical University, Tibet Autonomous Region, Lhasa 850000, China
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Abstract Objective To prove the protective effect and mechanism of Tibetan Medicine Ershiwuwei Feibing Pills on acute lung injury (ALI) rats. Methods A total of 84 SPF grade male SD rats (weighing [200±20] g, 6-8 weeks old) were divided by random number table into blank group, model group, Shuanghuanglian group (Shuanghuanglian Oral Solution 6 ml/kg), Dexamethasone group (2 mg/kg), and Ershiwuwei Feibing Pills high, medium, and low dose group (6.0, 3.0, 1.5 mg/kg) with 12 rats in each group. Except for the blank group, others were established by sublingual intravenous injection of lipopolysaccharide(LPS) (5 mg/kg). Administration by gavage 24 and 2 hours before modeling. The blood gases of the rats were measured by sampling blood from the abdominal aorta 24 h after modeling:partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), and pH value. Hematoxylin-Eeosin staining staining was used to observe lung histopathological changes and to perform lung injury histopathology score. ELISA detection of tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β), and interleukin-10 (IL-10) content in alveolar lavage fluid (BALF); lung tissue was analyzed by Western blot for Toll like receptor 4(TLR4), myeloid differentiation factor 88(MyD88), nuclear factor kappa-B(NF-κB), and myeloperoxidase (MPO) protein expression levels. Results Compared with the blank group, arterial blood PO2, PCO2, and pH value in the model group decreased (P＜0.05 or P＜0.01); compared with the model group, PO2 increased in the Ershiwuwei Feibing Pills high, medium dose groups, while PCO2 and pH value increased in the Ershiwuwei Feibing Pills high, medium and low dose groups (P＜0.05 or P＜0.01); compared with the Ershiwuwei Feibing Pills medium and low dose groups, PO2 in the Ershiwuwei Feibing Pills high dose group increased (P＜0.05). Compared with the blank group, the lung tissue of model group showed severe injury and significantly higher pathological scores(P＜0.01); compared with the model group, the lung tissue damage was reduced and the pathology score was significantly reduced in the Ershiwuwei Feibing Pills high, medium, and low dose groups (P＜0.01). Compared with the blank group, TNF-α, IL-1β, and IL-10 in the BALF of the model group increased (P＜0.01 or P＜0.05); compared with the model group, IL-1β and TNF-α content in the Ershiwuwei Feibing Pills high and medium dose groups significantly decreased (P＜0.01), but IL-10 increased (P＜0.05), and IL-1β content in the Ershiwuwei Feibing Pills low dose groups reduced (P＜0.05); compared with the Ershiwuwei Feibing Pills medium and low dose groups, IL-1β content in the Ershiwuwei Feibing Pills high dose group decreased, but IL-10 content increased (P＜0.05). Compared with the blank group, TLR4, MyD88, NF-κB, and MPO protein expression levels in the lung tissue of the model group significantly increased (P＜0.01); compared with the model group, TLR4, MyD88, NF-κB, and MPO protein expression levels in the Ershiwuwei Feibing Pill high, medium, and low dose groups significantly reduced(P＜0.01); compared with the Ershiwuwei Feibing Pills low dose group, TLR4, MyD88, and NF-κB protein expression levels in the Ershiwuwei Feibing Pills high dose group reduced (P＜0.05 or P＜0.01); compared with the Ershiwuwei Feibing Pills medium dose group, MyD88 protein expression level in the Ershiwuwei Feibing Pills high dose group significantly decreased (P＜0.01). Conclusion Ershiwuwei Feibing Pills can significantly improve LPS induced ALI in rats and its mechanism may be related to the regulation of TLR4/MyD88/NF-κB signaling pathway is related to reducing inflammation and the high-dose has the best effect.
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