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苏葶平喘汤对支气管哮喘大鼠的改善作用及机制
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| 篇名： | 苏葶平喘汤对支气管哮喘大鼠的改善作用及机制 |
| TITLE： | Improvement effects and mechanisms of Suting pingchuan decoction in rats with bronchial asthma |
| 摘要： | 目的 探讨苏葶平喘汤（STPC）对支气管哮喘大鼠的改善作用及潜在机制。方法将雄性SD大鼠分为空白组，模型组，STPC低、中、高剂量组（4.14、8.28、16.56g/kg，以生药量计），地塞米松组（阳性对照，1mg/kg），每组8只。除空白组外，其余各组以腹腔注射卵清蛋白致敏+雾化吸入卵清蛋白激发的方式构建支气管哮喘大鼠模型。自雾化激发之日起，各组大鼠在雾化前1h灌胃相应药液或生理盐水，每天1次，连续7d。实验期间，观察各组大鼠行为学变化；末次给药后，检测其支气管肺泡灌洗液（BALF）中炎症因子（白细胞介素1β、白细胞介素18）和肺组织中氧化应激指标[丙二醛（MDA）、超氧化物歧化酶（SOD）]水平，观察大鼠肺组织病理学改变，检测其肺组织细胞凋亡情况以及核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体3（NLRP3）mRNA和NLRP3、剪切型胱天蛋白酶1（cleavedcaspase-1）、胱天蛋白酶1（caspase-1）、消皮素D（GSDMD）、GSDMD氮端片段（GSDMD-N）蛋白的表达情况。结果与空白组比较，模型组大鼠出现抓耳挠腮、频繁打喷嚏等症状；肺组织结构严重受损，炎症细胞浸润明显；其BALF中炎症因子水平以及肺组织中MDA水平、TUNEL凋亡细胞率、NLRP3mRNA和NLRP3、cleavedcaspase-1、caspase-1、GSDMD-N、GSDMD蛋白的表达均显著升高或上调，肺组织中SOD水平显著降低（P＜0.05或P＜0.01）。与模型组比较，各药物组上述症状和肺组织病理损伤均明显改善，各定量指标（STPC各剂量组GSDMD蛋白表达，以及STPC低剂量组SOD水平和cleavedcaspase-1、caspase-1、GSDMD-N蛋白表达除外）均显著逆转（P＜0.05或P＜0.01）。结论STPC可改善支气管哮喘大鼠的气道炎症及肺组织损伤，降低氧化应激水平，减少IL-1β、IL-18等炎症因子的释放；其作用机制可能与抑制NLRP3/caspase-1/GSDMD介导的细胞焦亡通路活化有关。 |
| ABSTRACT： | OBJECTIVE To explore the improvement effects of Suting pingchuan decoction （STPC） on bronchial asthma in rats and its potential mechanism. METHODS Male SD rats were randomly divided into blank group， model group， STPC low-， medium- and high-dose groups （4.14， 8.28， and 16.56 g/kg， respectively， based on the crude drug dosage）， and dexamethasone group （positive control， 1 mg/kg）， with 8 rats in each group. Except for the blank group， the other groups were sensitized by intraperitoneal injection of ovalbumin and challenged by nebulized inhalation of ovalbumin to establish a bronchial asthma model. From the day of nebulization challenge， rats of each group were administered the corresponding drug solution or normal saline by gavage 1 hour before aerosolization， once a day， for 7 consecutive days. During the experiment， behavioral changes in rats of each group were observed. After the last administration， the levels of inflammatory factors （interleukin-1β， interleukin-18） in bronchoalveolar lavage fluid （BALF）， and oxidative stress indexes [malondialdehyde （MDA）， superoxide dismutase （SOD）] in lung tissue were determined； pathological changes in lung tissue were observed； cell apoptosis in lung tissue， and the mRNA expression of nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 （NLRP3） and the protein expressions of NLRP3， cleaved caspase-1， caspase-1， gasdermin D （GSDMD） and gasdermin D-N-terminal domain （GSDMD-N） in lung tissue were detected. RESULTS Compared with the blank group， rats in the model group showed symptoms such as scratching their ears and noses and frequent sneezing； the lung tissue structure was severely damaged， and there was obvious inflammatory cell infiltration. The levels of inflammatory factors in BALF， as well as the level of MDA， TUNEL-apoptotic cell rate， the mRNA expression of NLRP3， and the protein expressions of NLRP3， cleaved caspase-1， caspase-1， GSDMD-N and GSDMD in lung tissue were significantly increased or up-regulated， while the level of SOD in lung tissue was significantly decreased （ P ＜0.05 or P ＜0.01）. Compared with the model group， the above symptoms and pathological damages of lung tissue in each drug group were significantly improved， and all quantitative indicators （except for the protein expressions of GSDMD in the STPC groups， as well as the level of SOD， and the protein expressions of cleaved caspase-1， caspase-1 and GSDMD-N in the STPC low-dose group） were significantly reversed （ P ＜0.05 or P ＜0.01）. CONCLUSIONS STPC can improve airway inflammation and lung tissue damage in rats with bronchial asthma， reduce the level of oxidative stress， and decrease the release of inflammatory factors such as IL-1β and IL-18. Its mechanism of action may be related to the inhibition of pyroptosis activation mediated by the NLRP3/caspase-1/GSDMD signaling pathway. |
| 期刊： | 2026年第37卷第10期 |
| 作者： | 李梦茵；宋桂华；任明月；柴王猛 |
| AUTHORS： | LI Mengyin，SONG Guihua，REN Mingyue，CHAI Wangmeng |
| 关键字： | 苏葶平喘汤；支气管哮喘；氧化应激；细胞焦亡；NLRP3/caspase-1/GSDMD信号通路 |
| KEYWORDS： | Suting pingchuan decoction； bronchial asthma； oxidative stress； pyroptosis； NLRP3/caspase-1/GSDMD pathway |
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