Silibinin Mitigates Vanadium-induced Lung Injury via the TLR4/MAPK/NF-κB Pathway in Mice.

IF 1.8 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
In vivo Pub Date : 2024-09-01 DOI:10.21873/invivo.13681
Hobin Im, Eungyung Kim, Hong Ju Kwon, Hyeonjin Kim, Jiwon Ko, Yonghun Sung, Sung-Hyun Kim, Eun Jung Lee, Woo-Sung Kwon, Zae Young Ryoo, Junkoo Yi, Si Jun Park, Myoung Ok Kim
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引用次数: 0

Abstract

Background/aim: Silibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lung injury.

Materials and methods: Eight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts.

Results: Silibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils.

Conclusion: These findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants.

水飞蓟宾通过TLR4/MAPK/NF-κB途径减轻钒诱发的小鼠肺损伤
背景/目的:人们一直在研究西利宾在解决五氧化二钒(V2O5)诱导的肺部炎症方面的潜在益处和机制。本研究探讨了水飞蓟宾的抗炎活性,并阐明了水飞蓟宾在钒诱导的肺损伤小鼠模型中的作用机制:将八周大的雄性 BALB/c 小鼠暴露于 V2O5 以诱导肺损伤。对小鼠进行50毫克/千克和100毫克/千克剂量的西利宾预处理。对小鼠进行组织学分析,以评估细胞存活率和炎症细胞浸润情况。使用实时 PCR、Western 印迹分析和免疫组织化学方法评估了促炎细胞因子(TNF-α、IL-6、IL-1β)的表达、MAPK 和 NF-[式中:见正文]B 信号通路以及 NLRP3 炎性体的激活情况。全血分析用于测量白细胞计数:结果:在 V2O5 引起的肺损伤中,西利宾处理能明显提高细胞活力,减少炎症细胞浸润,降低促炎细胞因子的表达。它还明显抑制了 MAPK 和 NF-[配 方:见正文]B 信号通路的激活,同时明显降低了肺组织中 NLRP3 炎性体的表达水平。此外,西利宾处理组的白细胞数量也明显减少,包括中性粒细胞、淋巴细胞和嗜酸性粒细胞:这些发现强调了西利宾对 V2O5 诱导的肺部炎症小鼠的强效抗炎作用,凸显了其治疗潜力。这项研究不仅证实了丝利宾在减轻炎症反应方面的功效,还为人们了解丝利宾在调节关键炎症通路方面的作用提供了基础,为未来针对环境污染物诱发的肺部炎症的治疗策略铺平了道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
In vivo
In vivo 医学-医学:研究与实验
CiteScore
4.20
自引率
4.30%
发文量
330
审稿时长
3-8 weeks
期刊介绍: IN VIVO is an international peer-reviewed journal designed to bring together original high quality works and reviews on experimental and clinical biomedical research within the frames of physiology, pathology and disease management. The topics of IN VIVO include: 1. Experimental development and application of new diagnostic and therapeutic procedures; 2. Pharmacological and toxicological evaluation of new drugs, drug combinations and drug delivery systems; 3. Clinical trials; 4. Development and characterization of models of biomedical research; 5. Cancer diagnosis and treatment; 6. Immunotherapy and vaccines; 7. Radiotherapy, Imaging; 8. Tissue engineering, Regenerative medicine; 9. Carcinogenesis.
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