麻黄多糖通过调节肠道微生物群和短链脂肪酸减轻PM2.5和卵清蛋白诱导的小鼠哮喘样气道炎症。

Ephedra sinica polysaccharide alleviates airway inflammations of mouse asthma-like induced by PM2.5 and ovalbumin via the regulation of gut microbiota and short chain fatty acid.

作者信息

Liu Jun-Xi, Yuan Hong-Yu, Li Ya-Nan, Wei Zhen, Liu Yang, Liang Jun

机构信息

Key Laboratory of Basic and Application Research of Beiyao (Heilongjiang University of Chinese Medicine), Ministry of Education, Harbin, PR China.

Department of Pharmacy, Heilongjiang Nursing College, Harbin, PR China.

出版信息

J Pharm Pharmacol. 2022 Nov 25;74(12):1784-1796. doi: 10.1093/jpp/rgac078.

Abstract

OBJECTIVES

Epidemiological investigations show that long-term exposure to PM2.5 is directly related to asthma-like and other respiratory diseases. This study aims to further explore the pharmacological effect of Ephedra sinica polysaccharide (ESP) on lung injury caused by atmospheric PM2.5.

METHODS

To achieve the aim, we explored the therapeutic effect of ESP on an aggravated asthma-like mouse induced by PM2.5 combined with ovalbumin (OVA), and explored mechanisms underlying the connection between gut microbiota and lung function.

KEY FINDINGS

Preliminary results showed that ESP alleviated the symptoms of aggravated allergic asthma-like in mice; reduced the number of eosinophils in BALF; reduced the levels of serum Ig-E, IL-6, TNF-α, and IL-1β. Further qRT-PCR detected that ESP inhibited the NF-κB pathway. The final analysis detected by 16S rRNA and short chain fatty acid (SCFA) confirmed that ESP increased relative proportions of Bacteroides, Lactobacillus, Prevotella, Butyricicoccus and Paraprevotella, but decreased that of Enterococcus and Ruminococcus; increased acetic acid, propionic acid, butyric acid, isobutyric acid, valeric acid, isovaleric acid, and isohexanic acid in the meanwhile.

CONCLUSIONS

The study showed that ESP has a potential for future therapeutical applications in the prevention and treatment of asthma-like disease induced by PM2.5 and OVA via regulation of gut microbiota and SCFA.

摘要

目的

流行病学调查表明,长期暴露于细颗粒物(PM2.5)与哮喘样及其他呼吸道疾病直接相关。本研究旨在进一步探讨麻黄多糖(ESP)对大气PM2.5所致肺损伤的药理作用。

方法

为实现该目的,我们探究了ESP对由PM2.5联合卵清蛋白(OVA)诱导的哮喘样症状加重小鼠的治疗作用,并探究了肠道微生物群与肺功能之间联系的潜在机制。

主要发现

初步结果表明,ESP可缓解小鼠哮喘样症状加重的情况;减少支气管肺泡灌洗液(BALF)中嗜酸性粒细胞数量;降低血清免疫球蛋白E(Ig-E)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)水平。进一步的定量逆转录聚合酶链反应(qRT-PCR)检测发现,ESP可抑制核因子-κB(NF-κB)通路。通过16S核糖体RNA(rRNA)和短链脂肪酸(SCFA)进行的最终分析证实,ESP增加了拟杆菌属、乳杆菌属、普雷沃菌属、丁酸球菌属和副普雷沃菌属的相对比例,但降低了肠球菌属和瘤胃球菌属的比例;同时增加了乙酸、丙酸、丁酸、异丁酸、戊酸、异戊酸和异己酸的含量。

结论

该研究表明,ESP通过调节肠道微生物群和SCFA,在预防和治疗由PM2.5和OVA诱导的哮喘样疾病方面具有潜在的治疗应用前景。

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