首页|清肺汤通过PI3K/Akt信号通路对急性呼吸窘迫综合征大鼠细胞凋亡及Bcl-2、Bax表达的影响

清肺汤通过PI3K/Akt信号通路对急性呼吸窘迫综合征大鼠细胞凋亡及Bcl-2、Bax表达的影响

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目的 研究清肺汤参与急性呼吸窘迫综合征(ARDS)大鼠细胞凋亡过程、调控PI3K/Akt信号通路的作用机制.方法 SPF级大鼠共40只,随机分为空白组、模型组、清肺汤组、抑制剂组,每组10只.造模前1.5h,抑制剂组予渥曼青霉素1 mg/kg腹腔注射.除空白组外,各组大鼠均气管内滴注3 mg/kg脂多糖(LPS)100 μL造模,各组留置观察6 h后开始药物治疗.空白组、模型组给予灌胃蒸馏水12mL/kg,清肺汤组、抑制剂组灌胃清肺汤12 mL/kg;各组早晚各给药1次,连续7 d.干预结束后比较各组肺组织细胞凋亡情况及PI3K/Akt信号通路相关蛋白及Bax和Bcl-2基因表达情况.结果 模型组中大鼠肺组织中Bcl-2、磷酸化Akt和Gsk-3β表达明显低于空白组,Bax表达、肺组织中TUNEL阳性细胞率明显升高(P<0.05);抑制剂组中大鼠肺组织中Bcl-2、磷酸化Akt和Gsk-3β表达明显低于模型组,Bax表达、肺组织中TUNEL阳性细胞率明显升高(P<0.05),清肺汤组中肺组织中 Bax表达、肺组织中TUNEL阳性细胞率明显低于模型组和抑制剂组,Bel-2、磷酸化Akt和Gsk-3β表达明显高于模型组和抑制剂组(P<0.05).结论 清肺汤可能通过PI3K/Akt信号通路参与肺组织细胞凋亡过程治疗ARDS.
Effects of Qingfei Decoction on Cell Apoptosis and Bcl-2 and Bax Expression in Rats with Acute Respiratory Distress Syndrome through PI3K/Akt Signaling Pathway
Objective:To investigate the involvement of Qingfei Decoction in the process of cell apoptosis in rats with acute respiratory distress syndrome(ARDS)and the mechanism of regulating the PI3K/Akt signaling path-way.Methods:40 SPF level rats were randomly divided into a blank group,a model group,a Qingfei Decoction group,and an inhibitor group,with 10 rats in each group.One and a half hours before modeling,the inhibitor group was injected intraperitoneally with 1 mg/kg of wortmannin.Except for the blank group,the 30 rats were all given tracheal instillation of 3 mg/kg lipopolysaccharide(LPS)100 μL for modeling;each group was kept for obser-vation for 6 hours before starting drug treatment.The blank group and model group were given 12 mL/kg of dis-tilled water by gavage,while the Qingfei Decoction group and inhibitor group were given 12 mL/kg of Qingfei De-coction by gavage;each group was administered once in the morning and once in the evening for 7 consecutive days.After intervention,the apoptosis of lung tissue cells and the expression of PI3K/Akt signaling pathway relat-ed proteins,Bax,and Bcl-2 genes in each group were compared.Results:The expressions of Bcl-2,p-Akt,and p-Gsk-3β in the lung tissue of rats in the model group were significantly lower than those in the blank group,and the expression of Bax and the rate of TUNEL positive cells in lung tissue were significantly increased(P<0.05).The expressions of Bcl-2,p-Akt,and p-Gsk-3β in the lung tissue of rats in the inhibitor group were significantly lower than those in the model group,and the expression of Bax and the rate of TUNEL-positive cells in the lung tissue were significantly higher(P<0.05).The expression of Bax in the lung tissue and the rate of TUNEL-posi-tive cells in the lung tissue of the Qingfei Decoction group were significantly lower than those in the model group and the inhibitor group,and the expressions of Bcl-2,p-Akt,and p-Gsk-3β were significantly higher than those in the model group and the inhibitor group(P<0.05).Conclusion:Qingfei Decoction may participate in the pro-cess of lung tissue cell apoptosis through the PI3K/Akt signaling pathway in the treatment of ARDS.

Acute respiratory distress syndromeQingfei DecoctionApoptosisPI3K/Akt signaling pathwayLung tissueRats

王丛、张勤芹、薛宇菲

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江苏省南通市中医院,南京中医药大学南通附属医院,江苏南通 226000

急性呼吸窘迫综合征 清肺汤 细胞凋亡 P13K/Akt信号通路 肺组织 大鼠

南京中医药大学自然科学研究项目南通市科技计划南通市卫生计生委科研专项

XZR2020078JC2020005QA2021022

2024

中国中医急症
中华中医药学会

中国中医急症

CSTPCD
影响因子:1.144
ISSN:1004-745X
年,卷(期):2024.33(8)