异丙酚
下调和上调
细胞凋亡
基因表达
实时聚合酶链反应
分子生物学
体外
炎症
转化生长因子
基因
化学
药理学
生物
细胞生物学
免疫学
生物化学
作者
Fatemeh Sanie‐Jahromi,Mohammad Sadegh Sanie Jahromi
出处
期刊:Cornea
[Lippincott Williams & Wilkins]
日期:2023-09-13
卷期号:43 (1): 105-110
被引量:2
标识
DOI:10.1097/ico.0000000000003378
摘要
We investigated the effect of propofol (0.5, 5, and 50 μM) on the gene expression of inflammatory cytokines [ IL-1β , IL-6 , transforming growth factor β ( TGF-β ), and LIF ] and apoptosis process ( BCL-2 and Bax ) in corneal activated keratocytes (CAKs).CAKs (10 6 cells/10 cm 2 ) were exposed to propofol at a concentration of 0.5, 5, and 50 μM for 24 hours at 37°C. The control group did not receive propofol at the same time or under the same condition. Ribonucleic acid (RNA) extraction, complementary DNA (cDNA) synthesis, and real-time polymerase chain reaction (PCR) were performed to quantify the relative expression of IL-1β , IL-6 , TGF-β , LIF , BCL-2 , and Bax expression in the treated versus control cells.The results of this study showed that propofol treatment (0.5 and 5 μM) led to the downregulation of IL-1β and IL-6 gene expression in CAKs. TGF-β (with a role in fibrogenesis) was not changed in 0.5 and 5 μM propofol-treated CAKs, whereas CAKs treated with 50 μM propofol showed upregulation of the TGF-β gene. LIF (with a role in regeneration) was upregulated in 0.5 and 5 μM propofol-treated CAKs. The BCL-2/Bax ratio (as the antiapoptosis index) was increased in CAKs treated with 0.5 μM propofol and indicated the induction of an antiapoptotic effect.We showed that CAKs treatment with propofol, at concentrations of 0.5 and 5 μM, could decrease the expression of genes related to inflammation and enhance the genes associated with cell regeneration. While 50 μM propofol treatment might induce CAK fibrogenesis. This proof-of-concept study could preserve a groundwork for future drug design for the treatment of corneal stromal diseases and ocular regenerative medicine.
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