Green Tea Extract Reduced Lipopolysaccharide-Induced Inflammation in L2 Cells as Acute Respiratory Distress Syndrome Model Through Genes and Cytokine Pro-Inflammatory

Q3 Biochemistry, Genetics and Molecular Biology
D. Priyandoko, Wahyu Widowati, Lenny Lenny, Sintya Novianti, Revika Revika, Hanna Sari Widya Kusuma, Ika Adhani Sholihah
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Abstract

Background: Acute Respiratory Distress Syndrome (ARDS) is a severe lung inflammatory condition that has the capacity to impair gas exchange and lead to hypoxemia. This condition is found to have been one of the most prevalent in patients of COVID-19 with a more serious condition. Green tea (Camellia sinensis L.) contains polyphenols that possess many health benefits. The purpose of this study was to assess the anti-inflammatory activities of green tea extract in Lipopolysaccharide (LPS)-induced lung cells as ARDS cells model. Methods: In this study, rat lung cells (L2) were induced by LPS to mimic the inflammation observed in ARDS and later treated with green tea extract. Pro-inflammatory cytokines such as Interleukin (IL)-12, C-Reactive Protein (CRP) as well as Tumor Necrosis Factor-α (TNF-α) were investigated using the ELISA method. Gene expression of NOD-Like Receptor Protein 3 (NLRP-3), Receptor for Advanced Glycation End-product (RAGE), Toll-like Receptor-4 (TLR-4), and Nuclear Factor-kappa B (NF-κB) were evaluated by qRTPCR. Apoptotic cells were measured using flow cytometry. Results: The results showed that green tea extract treatment can reduce inflammation by suppressing gene expressions of NF-κB, NLRP-3, TLR-4, and RAGE, as well as pro-inflammatory cytokines such as IL-12, TNF-α, and CRP, an acute phase protein. Apoptosis levels of inflamed cells also found to be lowered when green tea extract was administered; thus, also increasing live cells compared to non-treated cells. Conclusion: These findings could lead to the future development of supplements from green tea to help alleviate ARDS symptoms, especially during critical moments such as the current pandemic.
绿茶提取物通过基因和细胞因子促炎作用降低急性呼吸窘迫综合征模型 L2 细胞中脂多糖诱导的炎症反应
背景:急性呼吸窘迫综合征(ARDS)是一种严重的肺部炎症,可损害气体交换并导致低氧血症。在病情更为严重的 COVID-19 患者中,这种情况最为普遍。绿茶(Camellia sinensis L.)含有多酚,对健康有很多益处。本研究旨在评估绿茶提取物在脂多糖(LPS)诱导的 ARDS 肺细胞模型中的抗炎活性。 研究方法本研究用 LPS 诱导大鼠肺细胞(L2),模拟 ARDS 中观察到的炎症,然后用绿茶提取物处理。采用 ELISA 方法检测白细胞介素(IL)-12、C 反应蛋白(CRP)和肿瘤坏死因子-α(TNF-α)等促炎细胞因子。通过 qRTPCR 评估了 NOD 样受体蛋白 3(NLRP-3)、高级糖化终产物受体(RAGE)、Toll 样受体-4(TLR-4)和核因子-卡巴 B(NF-κB)的基因表达。使用流式细胞术测量凋亡细胞。 结果显示结果表明,绿茶提取物能抑制 NF-κB、NLRP-3、TLR-4 和 RAGE 的基因表达,以及 IL-12、TNF-α 和 CRP(一种急性期蛋白)等促炎细胞因子,从而减轻炎症反应。研究还发现,服用绿茶提取物后,炎症细胞的凋亡水平也会降低;因此,与未服用绿茶提取物的细胞相比,活细胞数量也会增加。 结论这些发现可能会促使未来开发绿茶补充剂,以帮助缓解 ARDS 症状,尤其是在当前大流行病等关键时刻。
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
Avicenna journal of medical biotechnology
Avicenna journal of medical biotechnology Biochemistry, Genetics and Molecular Biology-Biotechnology
CiteScore
2.90
自引率
0.00%
发文量
43
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