Dataset Information

Galangin attenuates oxidative stress-mediated apoptosis in high glucose-induced renal tubular epithelial cells through modulating renin-angiotensin system and PI3K/AKT/mTOR pathway.

ABSTRACT: This study was to evaluate the regulatory network among Galangin (Gal), oxidative stress, and renin-angiotensin system (RAS) in diabetic nephropathy (DN) in vitro. A cell model of DN was set up by exposing HK-2 cells to high glucose (HG, 30 mM) for 48 h and Gal was applied at 10 μM when needed. mRNA expression was analyzed by qPCR and protein level was detected by western blot. Malondialdehyde level and superoxide dismutase activity were evaluated by commercial kits. We analyzed cell viability by CCK8 assay and apoptosis by flow cytometry. DCFH-DA staining was conveyed for reactive oxygen species detection. HG induced RAS activation, oxidative stress, while inhibited cell viability. Gal suppressed oxidative stress-mediated apoptosis of HK-2 cells under the stimulation of HG via inhibiting RAS activation. Moreover, overexpression of AT1R, a RAS gene, could restrain the mitigative effect of Gal on cell injury. Furthermore, repression of RAS induced by AT1R knockdown partially reversed HG-induced PI3K/AKT/mTOR activation and oxidative stress in HK-2 cells. Also, AKT activation could antagonize Gal's functional roles in renal cell damage. Collectively, Gal alleviates HG-induced oxidative stress injury of renal tubular epithelial cells through PI3K/AKT/mTOR signal via modulating RAS activation. This finding would help to better understand mechanism of DN development and support future studies.

SUBMITTER: Liao J

PROVIDER: S-EPMC8201591 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Galangin attenuates oxidative stress-mediated apoptosis in high glucose-induced renal tubular epithelial cells through modulating renin-angiotensin system and PI3K/AKT/mTOR pathway.

Liao Jie J Liu Bo B Chen Ke K Hu Sheng S Liu Zheng-Yu ZY Li Yu-Xin YX Yang Zhi-Ming ZM Zhang Meng M Chen Xiong X

Toxicology research 20210517 3

This study was to evaluate the regulatory network among Galangin (Gal), oxidative stress, and renin-angiotensin system (RAS) in diabetic nephropathy (DN) <i>in vitro</i>. A cell model of DN was set up by exposing HK-2 cells to high glucose (HG, 30 mM) for 48 h and Gal was applied at 10 μM when needed. mRNA expression was analyzed by qPCR and protein level was detected by western blot. Malondialdehyde level and superoxide dismutase activity were evaluated by commercial kits. We analyzed cell viab ...[more]

PMID: 34141169

Similar Datasets

Project description:Lung cancer is the most prevalent in cancer-related deaths, while breast carcinoma is the second most dominant cancer in women, accounting for the most number of deaths worldwide. Cancers are heterogeneous diseases that consist of several subtypes based on the presence or absence of hormone receptors and human epidermal growth factor receptor 2. Several drugs have been developed targeting cancer biomarkers; nonetheless, their efficiency are not adequate due to the high reemergence rate of cancers and fundamental or acquired resistance toward such drugs, which leads to partial therapeutic possibilities. Recent studies on cardiac glycosides (CGs) positioned them as potent cytotoxic agents that target multiple pathways to initiate apoptosis and autophagic cell death in many cancers. In the present study, our aim is to identify the anticancer activity of a naturally available CG (strophanthidin) in human breast (MCF-7), lung (A549), and liver cancer (HepG2) cells. Our results demonstrate a dose-dependent cytotoxic effect of strophanthidin in MCF-7, A549, and HepG2 cells, which was further supported by DNA damage on drug treatment. Strophanthidin arrested the cell cycle at the G2/M phase; this effect was further validated by checking the inhibited expressions of checkpoint and cyclin-dependent kinases in strophanthidin-induced cells. Moreover, strophanthidin inhibited the expression of several key proteins such as MEK1, PI3K, AKT, mTOR, Gsk3α, and β-catenin from MAPK, PI3K/AKT/mTOR, and Wnt/β-catenin signaling. The current study adequately exhibits the role of strophanthidin in modulating the expression of various key proteins involved in cell cycle arrest, apoptosis, and autophagic cell death. Our in silico studies revealed that strophanthidin can interact with several key proteins from various pathways. Taken together, this study demonstrates the viability of strophanthidin as a promising anticancer agent, which may serve as a new anticancer drug.

Dataset Information

Galangin attenuates oxidative stress-mediated apoptosis in high glucose-induced renal tubular epithelial cells through modulating renin-angiotensin system and PI3K/AKT/mTOR pathway.

Publications

Galangin attenuates oxidative stress-mediated apoptosis in high glucose-induced renal tubular epithelial cells through modulating renin-angiotensin system and PI3K/AKT/mTOR pathway.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets