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桔梗提取物通过 TLR4/NF-κBp65 通路减轻大鼠脂多糖诱导的急性肺损伤。

Platycodon grandiflorum extract attenuates lipopolysaccharide-induced acute lung injury via TLR4/NF-κBp65 pathway in rats.

机构信息

Sichuan Animal Science Academy, Chengdu, PR China/Animal Breeding and Genetics Key Laboratory of Sichuan Province, Chengdu, PR China.

Aba Teachers University, Wenchuan, PR China.

出版信息

Pak J Pharm Sci. 2021 Nov;34(6):2213-2218.

PMID:35034883
Abstract

The traditional Chinese medicine Platycodon grandiflorum (PG) is often used for the treatment of a number of chronic inflammatory diseases. In Chinese veterinary clinic, PG is always extracted by decoction and taken orally, however, the molecular mechanism of PG extract (PE) to reduce LPS-induced inflammation, especially acute lung injury (ALI) in vivo, are not known. Thus, we have studied the anti-inflammatory effects of PE on lipopolysaccharide (LPS)-induced acute lung injury via TLR4/NF-κBp65 pathway in rat. Sprague-Dawley rats were randomly divided into 4 groups: control group, LPS group, LPS±PE low dose group and LPS±PE high dose group. All rats were given corresponding PE solution or the same amount of normal saline by intragastric administration for 7 days. On the 7th day, 1 h after the last administration, 500 μg of LPS were introduced intratracheally to establish ALI rat model, and the same volume of normal saline was given to control group. The results showed that PE reduced the levels of LPS-induced pro-inflammatory mediators including IL-6, PGE2, and TNF-α, alleviated the lung injury histologically, and down-regulated LPS-induced mRNA and protein levels of TLR4/NF-κBp65 in lung tissue. This study demonstrated that PE has the anti-inflammatory effects on LPS-induced ALI in rats through TLR4/NF-κBp65 signaling pathway, indicating that PE is an effective suppressor for anti-inflammatory activities.

摘要

中药桔梗(PG)常被用于治疗多种慢性炎症性疾病。在中国兽医诊所,PG 通常通过煎煮和口服提取,但 PG 提取物(PE)在体内减轻 LPS 诱导的炎症,特别是急性肺损伤(ALI)的分子机制尚不清楚。因此,我们通过 TLR4/NF-κBp65 通路研究了 PE 对 LPS 诱导的急性肺损伤的抗炎作用。SD 大鼠随机分为 4 组:对照组、LPS 组、LPS+PE 低剂量组和 LPS+PE 高剂量组。所有大鼠均通过灌胃给予相应的 PE 溶液或等量生理盐水,连续 7 天。第 7 天,末次给药 1 h 后,经气管内注入 500 μg LPS 建立 ALI 大鼠模型,对照组给予等量生理盐水。结果表明,PE 降低了 LPS 诱导的促炎介质的水平,包括 IL-6、PGE2 和 TNF-α,减轻了肺组织的损伤,并下调了 LPS 诱导的肺组织 TLR4/NF-κBp65 的 mRNA 和蛋白水平。本研究表明,PE 通过 TLR4/NF-κBp65 信号通路对 LPS 诱导的 ALI 大鼠具有抗炎作用,表明 PE 是一种有效的抗炎活性抑制剂。

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