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肿瘤坏死因子-α,一条炎症途径,通过替代医学渠道重新定向。

TNF-α, An Inflammatory Path, Rerouted Through Alternate Medicinal Channels.

作者信息

Shanker Shyam Sundar, Kumar Krishna Santosh, Hussain Sharmila, Hariharan Annapoorni, Ramasamy Tamizhselvi

机构信息

Meenakshi Ammal Dental College and Hospital, Meenakshi Academy of Higher Education and Research (Deemed to be University), Chennai, Tamil Nadu, India.

Department of Biotechnology, School of Bioscience and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.

出版信息

J Pharm Bioallied Sci. 2024 Dec;16(Suppl 5):S4514-S4516. doi: 10.4103/jpbs.jpbs_1058_24. Epub 2025 Jan 30.

DOI:10.4103/jpbs.jpbs_1058_24
PMID:40061663
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11888719/
Abstract

INTRODUCTION

This study emphasizes the efficacy of triphala as a therapeutic agent over inflammatory condition in hydrogen sulfide (H S) mediated inflammatory path in the presence of titanium (Ti) discs.

MATERIALS AND METHOD

In the presence of triphala extracts, lipopolysaccharidetreated macrophages showed reduction in production of inflammatory mediators and intercellular free radicals (ROS) and downregulation of mRNA in TNF.

RESULTS

Thus in the presence of propargylglycine, reduction of TNFα by triphala in the H S inhibited group showed that the mechanism of action of triphala can be through the H S pathway.

摘要

引言

本研究强调了在存在钛(Ti)盘的情况下,三果木在硫化氢(H₂S)介导的炎症途径中作为治疗炎症病症的治疗剂的功效。

材料与方法

在三果木提取物存在的情况下,经脂多糖处理的巨噬细胞显示出炎症介质和细胞内自由基(ROS)产生的减少以及肿瘤坏死因子(TNF)中mRNA的下调。

结果

因此,在炔丙基甘氨酸存在的情况下,三果木在H₂S抑制组中对TNFα的降低表明三果木的作用机制可能是通过H₂S途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/732c58a0c4b7/JPBS-16-4514-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/fa73e0a8a737/JPBS-16-4514-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/3c9377f50332/JPBS-16-4514-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/732c58a0c4b7/JPBS-16-4514-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/fa73e0a8a737/JPBS-16-4514-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/3c9377f50332/JPBS-16-4514-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fec2/11888719/732c58a0c4b7/JPBS-16-4514-g003.jpg

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本文引用的文献

1
Death by TNF: a road to inflammation.肿瘤坏死因子致死:炎症之路。
Nat Rev Immunol. 2023 May;23(5):289-303. doi: 10.1038/s41577-022-00792-3. Epub 2022 Nov 15.
2
Triphala herbal extract suppresses inflammatory responses in LPS-stimulated RAW 264.7 macrophages and adjuvant-induced arthritic rats via inhibition of NF-κB pathway.三果草本提取物通过抑制NF-κB途径抑制脂多糖刺激的RAW 264.7巨噬细胞和佐剂诱导的关节炎大鼠的炎症反应。
J Immunotoxicol. 2016 Jul;13(4):509-25. doi: 10.3109/1547691X.2015.1136010. Epub 2016 Jul 20.
3
Evaluating the anti-inflammatory potential of Tectaria cicutaria L. rhizome extract in vitro as well as in vivo.
评价贯众根茎提取物的体外抗炎活性及其体内活性。
J Ethnopharmacol. 2013 Oct 28;150(1):215-22. doi: 10.1016/j.jep.2013.08.025. Epub 2013 Aug 27.
4
The effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages.硫化氢供体对脂多糖诱导的巨噬细胞中炎症介质形成的影响。
Antioxid Redox Signal. 2010 May 15;12(10):1147-54. doi: 10.1089/ars.2009.2899.