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Pigment epithelium-derived factor may play a role in apoptosis of human liver cells induced by arsenic through regulating Bcl-2 level / 中华地方病学杂志
Chinese Journal of Endemiology ; (12): 623-626, 2018.
Artigo em Chinês | WPRIM | ID: wpr-701390
ABSTRACT
Objective To explore the mechanism of pigment epithelium-derived factor (PEDF) on human liver cells in mitochondrial apoptosis induced by arsenic. Methods Human normal liver cell line (HHL-5) was exposed to NaAsO2 for 24 h, the dose was 0 (control), 2, 5, 8 and 10 μmol/L, respectively. The mitochondrial membrane potential was determined by using flow cytometry, and mRNA levels of PEDF, Bcl-2 and Bax were assayed by Real-time fluorescent quantitative PCR. Results The mitochondrial membrane potential in 10 μmol/L arsenic group (562.33 ± 31.50) was decreased markedly in comparison with that of control group (688.67 ± 47.50, P<0.01), the levels in other groups (5 μmol/L 634.50 ± 49.03, 8 μmol/L 655.67 ± 13.65) were not significantly changed (P > 0.05). Compared with control group [(86.69 ± 12.19)%], the mRNA levels of PEDF decreased significantly (P<0.01) when the HHL-5 cells were cultivated with 5 μmol/L [(59.35 ± 11.21)%], 8μmol/L [(58.46 ± 8.69)%] and 10μmol/L [(51.57 ± 7.58)%] arsenic, respectively, and the PEDF mRNA level in 10 μmol/L group was the lowest; but there was no significant change in PEDF mRNA level [(81.52 ± 13.93)%] when HHL-5 cell was cultivated with 2μmol/L arsenic. Similarly, mRNA level of Bcl-2 in 10 μmol/L arsenic group [(53.53 ± 21 . 49 )%] was significantly decreased compared with that of the control group [(96.48 ± 31.14)%, P < 0.05]. Whereas, Bax mRNA levels in arsenic exposure groups [(65.14 ± 32.34)%, (71.81 ± 12.61)%, (72.22 ± 28.40)%] were not significantly changed in comparison with that of control group [(84.47 ± 35.38)%, P > 0.05]. Conclusion PEDF may play a role in mitochondrial apoptosis of human liver cells induced by arsenic through regulating Bcl-2 level.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Endemiology Ano de publicação: 2018 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Endemiology Ano de publicação: 2018 Tipo de documento: Artigo