Department of respiration, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100000, China.
2 Department of traditional Chinese Medicine, Peking University People's Hospital, Beijing, 100000, China.
J Tradit Chin Med. 2022 Apr;42(2):200-212. doi: 10.19852/j.cnki.jtcm.20211214.004.
To explore the effect and mechanism of baicalin in the treatment of acute lung injury (ALI) by and experiments.
ALI was induced by instilling 10 mg/mL lipopolysaccharide (LPS) into the airway of rats. Different doses of baicalin (50 and 100 mg·kg ·d) were administered by gavage one day before modeling.
Baicalin significantly reduced the permeability of the alveolocapillary membrane, alleviated tissue injury and inflammatory infiltration, and inhibited the secretion of inflammatory factors and the infiltration of neutrophils. The decline in these inflammations was related to the inhibition of the toll like receptor-4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB)/nod-like receptor pyrin containing 3 (NLRP3) signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathway.
Baicalin inhibits the secretion of inflammatory factors by inhibiting the TLR4-MyD88-NF-κB/NLRP3 pathway and the MAPK signaling pathway. Thus, it reduces lung bronchial epithelial layer, alveolar damage, and pulmonary edema as detected in the and experiments. Therefore, baicalin may be a potential preventive and therapeutic drug for ALI.
通过实验探索黄芩苷治疗急性肺损伤（ALI）的作用及机制。
通过向大鼠气道滴注 10mg/mL 脂多糖（LPS）诱导 ALI，造模前 1 天灌胃给予不同剂量的黄芩苷（50 和 100mg·kg·d）。
黄芩苷显著降低了肺泡毛细血管膜的通透性，减轻了组织损伤和炎症浸润，并抑制了炎症因子的分泌和中性粒细胞的浸润。这些炎症的下降与抑制 toll 样受体 4（TLR4）/髓样分化因子 88（MyD88）/核因子-κB（NF-κB）/含核苷酸结合寡聚化结构域受体 3（NLRP3）信号通路和丝裂原活化蛋白激酶（MAPK）信号通路有关。
黄芩苷通过抑制 TLR4-MyD88-NF-κB/NLRP3 途径和 MAPK 信号通路抑制炎症因子的分泌，从而减少肺支气管上皮层、肺泡损伤和肺水肿，这在实验中得到了验证。因此，黄芩苷可能是 ALI 的一种潜在预防和治疗药物。
