sirolimus and hydroquinone

sirolimus has been researched along with hydroquinone* in 1 studies

Other Studies

1 other study(ies) available for sirolimus and hydroquinone

Article	Year
Inhibition of autophagy enhances Hydroquinone-induced TK6 cell death. Toxicology in vitro : an international journal published in association with BIBRA, 2017, Volume: 41 Hydroquinone (HQ), one of the metabolic products of benzene, is a carcinogen. It can induce apoptosis in lymphoma cells. However, whether HQ can induce autophagy and what roles autophagy plays in TK6 cells exposured to HQ remains unclear. In this study, we found that HQ could induce autophagy through techniques of qRT-PCR, Western blot, immunofluorescent assay of LC3 and transmission electron microscope. Furthermore, inhibiting autophagy using 3-methyladenine (3-MA) or chloroquine (CQ) significantly enhanced HQ-induced cell apoptosis, suggesting that autophagy may be a survival mechanism. Our study also showed that HQ activated PARP-1. Moreover, knockdown of PARP-1 strongly exhibited decreased autophagy related genes expression. In contrast, the absence of SIRT1 increased that. Altogether, our data provided evidence that HQ induced autophagy in TK6 cells and autophagy protected TK6 from HQ attack-induced injury in vitro, and the autophagy was partially mediated via activation of the PARP-1-SIRT1 signaling pathway. Topics: Adenine; Apoptosis; Autophagy; Autophagy-Related Protein 5; Beclin-1; Cell Line; Chloroquine; Gene Knockdown Techniques; Humans; Hydrogen Peroxide; Hydroquinones; Microtubule-Associated Proteins; Poly (ADP-Ribose) Polymerase-1; Sirolimus; Sirtuin 1	2017

Article

Year

Inhibition of autophagy enhances Hydroquinone-induced TK6 cell death.

Toxicology in vitro : an international journal published in association with BIBRA, 2017, Volume: 41

Hydroquinone (HQ), one of the metabolic products of benzene, is a carcinogen. It can induce apoptosis in lymphoma cells. However, whether HQ can induce autophagy and what roles autophagy plays in TK6 cells exposured to HQ remains unclear. In this study, we found that HQ could induce autophagy through techniques of qRT-PCR, Western blot, immunofluorescent assay of LC3 and transmission electron microscope. Furthermore, inhibiting autophagy using 3-methyladenine (3-MA) or chloroquine (CQ) significantly enhanced HQ-induced cell apoptosis, suggesting that autophagy may be a survival mechanism. Our study also showed that HQ activated PARP-1. Moreover, knockdown of PARP-1 strongly exhibited decreased autophagy related genes expression. In contrast, the absence of SIRT1 increased that. Altogether, our data provided evidence that HQ induced autophagy in TK6 cells and autophagy protected TK6 from HQ attack-induced injury in vitro, and the autophagy was partially mediated via activation of the PARP-1-SIRT1 signaling pathway.

Topics: Adenine; Apoptosis; Autophagy; Autophagy-Related Protein 5; Beclin-1; Cell Line; Chloroquine; Gene Knockdown Techniques; Humans; Hydrogen Peroxide; Hydroquinones; Microtubule-Associated Proteins; Poly (ADP-Ribose) Polymerase-1; Sirolimus; Sirtuin 1

2017