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6 results on '"Pan, Jigang"'

5. Peperomin E Induces Apoptosis and Cytoprotective Autophagy in Human Prostate Cancer DU145 Cells In Vitro and In Vivo.

Author

Lin, Min, Zhu, Qiannan, Li, Yunzhi, and Pan, Jigang

Subjects
IN vitro studies, FLOW cytometry, IN vivo studies, XENOGRAFTS, AUTOPHAGY, ANIMAL experimentation, MICROSCOPY, WESTERN immunoblotting, ANTINEOPLASTIC agents, APOPTOSIS, GENE expression, TREATMENT effectiveness, CELL proliferation, PLANT extracts, CELL lines, PROSTATE tumors, MICE, PHARMACODYNAMICS
Abstract

Peperomin E was first isolated from Peperomia dindygulensis , an anticarcinogenic herb, and exhibited anticancer activity in many cancer cell lines. To date, it is unknown whether peperomin E has an effect on human prostate cancer DU145 cells in vitro and in vivo. In this study, we used MTT to assess the proliferation inhibition activity of peperomin E in DU145 cells in vitro and observed the cell morphological changes by a phase contrast microscope. A DU145 cell xenograft tumor mouse model was used to evaluate the efficacy of peperomin E in vivo. Apoptosis rates were measured by flow cytometry, and protein expression levels were analyzed by western blot. The results showed that peperomin E significantly inhibited the proliferation of DU145 cells in vitro and reduced the weight and volume of tumors in vivo. Peperomin E also significantly induced the apoptosis and autophagic response of DU145 cells. The autophagic inhibitors LY294002 and chloroquine enhanced peperomin E-mediated inhibition of DU145 cell proliferation and induction of DU145 cell apoptosis. The results also showed that the Akt/mTOR pathway participated in peperomin E-induced autophagy in DU145 cells. In summary, our finding showed that peperomin E had an effect on DU145 cells in vitro and in a nude mouse DU145 cell xenograft model in vivo , demonstrated that peperomin E could significantly induce apoptosis and the autophagic response in DU145 cells and that autophagy played a cytoprotective role in peperomin E-treated DU145 cells. These results suggest that the combination of peperomin E treatment and autophagic inhibition has potential for the treatment of prostate cancer. [ABSTRACT FROM AUTHOR]

Published
2021
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6. Hydrogen Sulfide Promotes Postnatal Cardiomyocyte Proliferation by Upregulating SIRT1 Signaling Pathway.

Author

Gan L, Cheng P, Wu J, Li Q, Pan J, Ding Y, Gao X, and Chen L

Subjects
Animals, Mice, Animals, Newborn, Cells, Cultured, Mice, Inbred C57BL, Sulfides, Sirtuin 1 metabolism, Hydrogen Sulfide pharmacology, Hydrogen Sulfide metabolism, Cell Proliferation drug effects, Myocytes, Cardiac drug effects, Myocytes, Cardiac metabolism, Up-Regulation, Signal Transduction drug effects
Abstract

Hydrogen sulfide (H 2 S) has been identified as a novel gasotransmitter and a substantial antioxidant that can activate various cellular targets to regulate physiological and pathological processes in mammals. However, under physiological conditions, it remains unclear whether it is involved in regulating cardiomyocyte (CM) proliferation during postnatal development in mice. This study mainly aimed to evaluate the role of H 2 S in postnatal CM proliferation and its regulating molecular mechanisms. We found that sodium hydrosulfide (NaHS, the most widely used H 2 S donor, 50-200 μM) increased neonatal mouse primary CM proliferation in a dose-dependent manner in vitro. Consistently, exogenous administration of H 2 S also promoted CM proliferation and increased the total number of CMs at postnatal 7 and 14 days in vivo. Moreover, we observed that the protein expression of SIRT1 was significantly upregulated after NaHS treatment. Inhibition of SIRT1 with EX-527 or si-SIRT1 decreased CM proliferation, while enhancement of the activation of SIRT1 with SRT1720 promoted CM proliferation. Meanwhile, pharmacological and genetic blocking of SIRT1 repressed the effect of NaHS on CM proliferation. Taken together, these results reveal that H 2 S plays a promotional role in proliferation of CMs in vivo and in vitro and SIRT1 is required for H 2 S-mediated CM proliferation, which indicates that H 2 S may be a potential modulator for heart development in postnatal time window.

Published
2024
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