Biochemistry and biophysics reports · 2025
The miR-146a-associated HDAC2 regulation of PI3K is involved in pancreatitis in vitro.
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Zhong Ding-Wen, Zeng Xiang-Tian, Chen Wen-Hui, Huang Xian-Yu, Liu Jia-Xin, Liao Yong-Hui
Аннотация
PURPOSE: To investigate the association between miR-146a/HDAC2 and their regulatory roles on the PI3K expression during pancreatitis.
METHODS: Rat pancreatic AR42J cells were treated with LPS for simulating pancreatitis. Expression levels of inflammatory factors (IL-6, TNF-α) and miR-146a were detected to determine the optimal LPS concentration for establishing an in vitro pancreatitis model. Cell proliferation and apoptosis were analyzed using CCK-8 and flow cytometry. Immunofluorescence was performed to assess co-localization of HDAC2 and PI3K. ELISA quantified TNF-α and IL-6 levels in cell supernatants. A dual-luciferase assay verified the targeting relationship between miR-146a and HDAC2.
RESULTS: Compared to controls, the cell proliferation ability of the pancreatitis model group was decreased, whereas TSA and miR-146a mimic interventions restored proliferation. The expression of IL-6 and TNF-αin the LPS group was higher than that in the control group, and their expression decreases in the TSA and miR-146a mimic intervention group. Besides the dual luciferase detected the targeting relationship between miR-146a and HDAC2, the immunofluorescence showed co-localization of HDAC2 and PI3K.
CONCLUSIONS: TSA and miR-146a mimic enhance proliferation and reduce inflammation in pancreatitis cells. The miR-146a/HDAC2 axis may mediate therapeutic effects in pancreatitis by modulating the PI3K expression.
METHODS: Rat pancreatic AR42J cells were treated with LPS for simulating pancreatitis. Expression levels of inflammatory factors (IL-6, TNF-α) and miR-146a were detected to determine the optimal LPS concentration for establishing an in vitro pancreatitis model. Cell proliferation and apoptosis were analyzed using CCK-8 and flow cytometry. Immunofluorescence was performed to assess co-localization of HDAC2 and PI3K. ELISA quantified TNF-α and IL-6 levels in cell supernatants. A dual-luciferase assay verified the targeting relationship between miR-146a and HDAC2.
RESULTS: Compared to controls, the cell proliferation ability of the pancreatitis model group was decreased, whereas TSA and miR-146a mimic interventions restored proliferation. The expression of IL-6 and TNF-αin the LPS group was higher than that in the control group, and their expression decreases in the TSA and miR-146a mimic intervention group. Besides the dual luciferase detected the targeting relationship between miR-146a and HDAC2, the immunofluorescence showed co-localization of HDAC2 and PI3K.
CONCLUSIONS: TSA and miR-146a mimic enhance proliferation and reduce inflammation in pancreatitis cells. The miR-146a/HDAC2 axis may mediate therapeutic effects in pancreatitis by modulating the PI3K expression.