Baicalin relieves complement alternative pathway activation-induced lung inflammation through inhibition of NF-κB pathway.

IF 3.3 2区 医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE BMC Complementary Medicine and Therapies Pub Date : 2024-09-13 DOI:10.1186/s12906-024-04622-y
Jiao Li, Qi-Yun Zhang, Qing-Yu Lu, Qiao-Zhou Liu, Li Guo, Min Li, Qian-Yun Sun
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Abstract

Introduction: Acute lung injury (ALI) as one kind of acute pulmonary inflammatory disorder, manifests primarily as damage to alveolar epithelial cells and microvascular endothelial cells. Activation of the complement system is a common pathological mechanism in ALI induced by diverse factors, with the complement alternative pathway assuming a pivotal role. Baicalin, a flavonoid derived from the root of Scutellaria baicalensis Georgi, exhibits noteworthy biological activities. The present study attempted the interventional effects and underlying mechanisms of baicalin in microangiopathy in ALI induced by complement alternative pathway activation.

Methods: Activation of the complement alternative pathway by cobra venom factor (CVF). HMEC cells were pretreated with baicalin and then exposed to complement activation products. The expression of inflammatory mediators was detected by ELISA, and the intranuclear transcriptional activity of NF-κB was assessed by a dual fluorescent kinase reporter gene assay kit. Before establishing the ALI mouse model, baicalin or PDTC was gavaged for 7 d. CVF was injected into the tail vein to establish the ALI model. The levels of inflammatory mediators in BALF and serum were determined by ELISA. HE staining and immunohistochemistry evaluated pathological changes, complement activation product deposition, and NF-κB p65 phosphorylation in lung tissue.

Results: Baicalin reduced complement alternative activation product-induced expression of HMEC cells adhesion molecules (ICAM-1, VCAM-1, E-selectin) and cytokines (IL-6, TNF-α) as well as upregulation of NF-κB intranuclear transcriptional activity. Baicalin intervention reduced the number of inflammatory cells and protein content in the BALF and decreased the levels of IL-6, TNF-α, and ICAM-1 in serum and IL-6, TNF-α, ICAM-1, and P-selectin in BLAF. In addition, baicalin attenuated inflammatory cell infiltration in the lung of ALI mice and reduced the deposition of complement activation products (C5a, C5b-9) and phosphorylation of NF-κB p65 in lung tissue.

Conclusion: Baicalin relieves complement alternative pathway activation-induced lung inflammation by inhibition of NF-κB pathway, delaying the progression of ALI.

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黄芩苷通过抑制 NF-κB 通路缓解补体替代通路激活引起的肺部炎症
导言急性肺损伤(ALI)是急性肺部炎症性疾病的一种,主要表现为肺泡上皮细胞和微血管内皮细胞的损伤。补体系统激活是多种因素诱发 ALI 的常见病理机制,其中补体替代途径起着关键作用。黄芩苷是从黄芩(Scutellaria baicalensis Georgi)根中提取的一种黄酮类化合物,具有显著的生物活性。本研究试图探讨黄芩苷对补体替代途径激活诱导的 ALI 微血管病变的干预作用及其内在机制:方法:眼镜蛇毒因子(CVF)激活补体替代途径。用黄芩苷预处理 HMEC 细胞,然后将其暴露于补体激活产物中。用 ELISA 检测炎症介质的表达,用双荧光激酶报告基因检测试剂盒评估 NF-κB 的核内转录活性。在建立 ALI 小鼠模型之前,先用黄芩苷或 PDTC 灌胃 7 d。用 ELISA 法测定 BALF 和血清中的炎症介质水平。HE 染色和免疫组化评估了肺组织的病理变化、补体活化产物沉积和 NF-κB p65 磷酸化:结果:黄芩苷减少了补体替代活化产物诱导的 HMEC 细胞粘附分子(ICAM-1、VCAM-1、E-选择素)和细胞因子(IL-6、TNF-α)的表达,以及 NF-κB 核内转录活性的上调。黄芩苷干预可减少 BALF 中炎症细胞的数量和蛋白质含量,降低血清中 IL-6、TNF-α 和 ICAM-1 的水平,以及 BLAF 中 IL-6、TNF-α、ICAM-1 和 P-selectin 的水平。此外,黄芩苷还能减轻 ALI 小鼠肺部的炎症细胞浸润,减少补体激活产物(C5a、C5b-9)的沉积和肺组织中 NF-κB p65 的磷酸化:结论:黄芩苷可通过抑制 NF-κB 通路缓解补体替代通路激活诱导的肺部炎症,从而延缓 ALI 的进展。
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来源期刊
BMC Complementary Medicine and Therapies
BMC Complementary Medicine and Therapies INTEGRATIVE & COMPLEMENTARY MEDICINE-
CiteScore
6.10
自引率
2.60%
发文量
300
审稿时长
19 weeks
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