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尤那尼配方药物库尔思·萨尔坦·卡富里抗分枝杆菌作用的机制研究

Mechanistic insights into the antimycobacterial action of unani formulation, Qurs Sartan Kafoori.

作者信息

Hameed Saif, Hans Sandeep, Nandan Shiv, Fatima Zeeshan

机构信息

Amity Institute of Biotechnology, Amity University Haryana, Manesar, Gurugram, 122413, India.

Amity Lipidomics Research Facility, Amity University Haryana, Manesar, Gurugram, 122413, India.

出版信息

J Tradit Complement Med. 2021 Jul 30;12(2):162-171. doi: 10.1016/j.jtcme.2021.07.009. eCollection 2022 Mar.

DOI:10.1016/j.jtcme.2021.07.009
PMID:35528471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9072819/
Abstract

BACKGROUND AND AIM

Tuberculosis (TBC) is a deadly disease and major health issue in the world. Emergence of drug resistant strains further worsens the efficiency of available anti-TBC drugs. Natural compounds and particularly traditional medicines such as Unani drugs are one of the promising alternatives that have been widely used nowadays. This study aims to evaluate the efficacy of unani drug Qurs-e-Sartan Kafoori (QSK) on (MTB).

EXPERIMENTAL PROCEDURES

Drug susceptibilities were estimated by broth microdilution assay. Cell surface integrity was assessed by ZN staining, colony morphology and nitrocefin hydrolysis. Biofilms were visualized by crystal violet staining and measurement of metabolic activity and biomass. Lipidomics analysis was performed using mass spectrometry. Host pathogen interaction studies were accomplished using THP-1 cell lines to estimate cytokines by ELISA kit, apoptosis and ROS by flow cytometry.

RESULTS

QSK enhanced the susceptibilities of isoniazid and rifampicin and impaired membrane homeostasis as depicted by altered cell surface properties and enhanced membrane permeability. In addition, virulence factor, biofilm formation was considerably reduced in presence of QSK. Lipidomic analysis revealed extensive lipid remodeling. Furthermore, we used a THP-1 cell line model, and investigated the immunomodulatory effect by estimating cytokine profile and found change in expressions of TNF-α, IL-6 and IL-10. Additionally, we uncover reduced THP-1 apoptosis and enhanced ROS production in presence of QSK.

CONCLUSION

Together, this study validates the potential of unani formulation (QSK) with its mechanism of action and attempts to highlight its significance in MDR reversal.

摘要

背景与目的

结核病是一种致命疾病,也是全球主要的健康问题。耐药菌株的出现进一步降低了现有抗结核药物的疗效。天然化合物,特别是传统药物如尤那尼药物,是目前广泛使用的有前景的替代药物之一。本研究旨在评估尤那尼药物库尔思 - 萨坦卡富里(QSK)对结核分枝杆菌(MTB)的疗效。

实验步骤

通过肉汤微量稀释法评估药物敏感性。通过齐 - 尼染色、菌落形态和硝基头孢菌素水解评估细胞表面完整性。通过结晶紫染色以及代谢活性和生物量的测量观察生物膜。使用质谱进行脂质组学分析。利用THP - 1细胞系进行宿主 - 病原体相互作用研究,通过酶联免疫吸附测定试剂盒评估细胞因子,通过流式细胞术评估细胞凋亡和活性氧。

结果

QSK增强了异烟肼和利福平的敏感性,并破坏了膜稳态,表现为细胞表面特性改变和膜通透性增强。此外,在QSK存在的情况下,毒力因子生物膜形成显著减少。脂质组学分析显示广泛的脂质重塑。此外,我们使用THP - 1细胞系模型,通过评估细胞因子谱研究免疫调节作用,发现肿瘤坏死因子 - α、白细胞介素 - 6和白细胞介素 - 10的表达发生变化。此外,我们发现在QSK存在的情况下,THP - 1细胞凋亡减少,活性氧生成增加。

结论

总之,本研究验证了尤那尼制剂(QSK)的潜力及其作用机制,并试图突出其在耐多药逆转中的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/3059b0dc8bf8/gr8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/5d94485148c6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/18f36ab9a093/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/c9c96f416185/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/e13125939ca8/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/b072cda7aebc/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/3059b0dc8bf8/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/7962e206a860/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/0b1877880222/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/28aad2072fad/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/5d94485148c6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/18f36ab9a093/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/c9c96f416185/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/e13125939ca8/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/b072cda7aebc/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b89/9072819/3059b0dc8bf8/gr8.jpg

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