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奥克欣对大鼠肝星状细胞的抗纤维化和凋亡作用。

Antifibrogenic and apoptotic effects of Ocoxin in cultured rat hepatic stellate cells.

机构信息

Department of Biochemistry and Genetics, University of Navarra, 31008, Pamplona, Spain.

出版信息

J Physiol Biochem. 2023 Nov;79(4):881-890. doi: 10.1007/s13105-022-00878-5. Epub 2022 Mar 3.

DOI:10.1007/s13105-022-00878-5
PMID:35239161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10635942/
Abstract

Ocoxin is a nutritional supplement that has been shown to exert antioxidant and immunomodulatory responses in patients with chronic hepatitis C. The present work aimed to determine the effects of Ocoxin on activated hepatic stellate cells (HSC), the cell type mainly responsible for collagen deposition in the fibrotic liver. Ocoxin was found to reduce the survival of a cell line of immortalized non-tumoral rat HSC in a dose-response fashion and to diminish collagen type I levels. This latter effect was observed even at doses not affecting cell survival, pointing to an antifibrogenic action for the supplement. The decrease in viability exerted by Ocoxin on HSC correlated with an increase in histone-associated fragments in the cytoplasm and with increased activity of caspase-3, indicating the induction of apoptosis. To determine the molecular mechanisms mediating Ocoxin-induced apoptosis, the activation of members of the MAPK family was analyzed. Incubation of HSC with Ocoxin caused a transient and dramatic enhancement on ERK, JNK, and p38 MAPK phosphorylation levels. Using specific inhibitors for these enzymes, p38 MAPK was identified as a key mediator of the apoptotic effect of Ocoxin on HSC.

摘要

奥克辛是一种营养补充剂，已被证明能在慢性丙型肝炎患者中发挥抗氧化和免疫调节作用。本研究旨在确定奥克辛对活化的肝星状细胞（HSC）的影响，HSC 是肝纤维化过程中胶原沉积的主要细胞类型。结果发现，奥克辛以剂量依赖的方式降低了永生化非肿瘤大鼠 HSC 细胞系的存活率，并减少了 I 型胶原的水平。即使在不影响细胞存活的剂量下也观察到了这种作用，这表明该补充剂具有抗纤维化作用。奥克辛对 HSC 活力的降低与细胞质中组蛋白相关片段的增加以及 caspase-3 活性的增加有关，表明诱导了细胞凋亡。为了确定介导奥克辛诱导凋亡的分子机制，分析了 MAPK 家族成员的激活。用奥克辛孵育 HSC 会导致 ERK、JNK 和 p38 MAPK 磷酸化水平短暂而显著增强。使用这些酶的特异性抑制剂，鉴定出 p38 MAPK 是奥克辛诱导 HSC 凋亡的关键介质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/3f85a5b908b7/13105_2022_878_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/92c4f6fb82f0/13105_2022_878_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/b111b41f984d/13105_2022_878_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/02cbdeb5ae9a/13105_2022_878_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/8db5e107b2fa/13105_2022_878_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/ff01041bd613/13105_2022_878_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/3f85a5b908b7/13105_2022_878_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/92c4f6fb82f0/13105_2022_878_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/b111b41f984d/13105_2022_878_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/2cc902b265da/13105_2022_878_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/02cbdeb5ae9a/13105_2022_878_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/8db5e107b2fa/13105_2022_878_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/ff01041bd613/13105_2022_878_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51a2/10635942/3f85a5b908b7/13105_2022_878_Fig7_HTML.jpg

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