Abstract:
Objective To investigate the role and mechanism of long non-coding RNA-TC(Lnc-TC)in benzene-induced hematotoxicity toxicity.
Methods Different doses of benzene metabolite, 1, 4-benzoquinone (1, 4-BQ) were used in vitro to treat human B lymphocytes (AHH-1) for 24 h. Cell viability was detected by MTT method. Transmission electron microscope and immunofluorescence method were used to detect cell apoptosis, and qRT-PCR was used to detect the expression of Lnc-TC and the apoptosis-related gene caspase-3. The Lnc-TC interference model was constructed by lentivirus in vitro to explore the effect on cell apoptosis.
Results The results of cell experiments showed that 1, 4-BQ reduced the viability of AHH-1 cells in a dose-dependent manner, leading to abnormal cell morphology, and the appearance of apoptotic bodies was accompanied by the up-regulation of the expression of caspase-3, the apoptotic executive gene. At the same time, 1, 4-BQ induced a significant up-regulation of the Lnc-TC expression. After interfering with Lnc-TC, it was found that interfering with Lnc-TC alleviated cell apoptosis and reversed the up-regulation of caspase-3 expression caused by 1, 4-BQ.
Conclusion Lnc-TC induces cell apoptosis and leads to benzene hemotoxicity by regulating the expression of the apoptosis executive gene caspase-3.