Mouse recombinant leptin protects human hepatoma HepG2 against apoptosis, TNF-α response and oxidative stress induced by the hepatotoxin–ethanol

Vairappan, Balasubramaniyan; Shukla, Ruchi; Murugaiyan, Gopal; Bhonde, Ramchandra Ramesh; Nalini, Namasivayam

doi:10.1016/j.bbagen.2007.04.009

Cited by 30 publications

(20 citation statements)

References 42 publications

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“…HepG2 cell line has been proposed as a good model to study in vitro toxicity to the liver since it retains many of the specialized functions (Akanitapichat et al 2010;Balasubramaniyan et al 2007). We first studied the response of HepG2 cells to CCl 4 dose by MTT assay and flow cytometry.…”

Section: Effect Of Isolated Compounds On Viability Of CCL 4 -Induced mentioning

confidence: 99%

Hepatoprotective effect of phenylethanoid glycosides from Incarvillea compacta against CCl4-induced cytotoxicity in HepG2 cells

Shen

Zhang

et al. 2015

J Korean Soc Appl Biol Chem

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The extraction and solvent partition of roots of Incarvillea compacta, a traditional Tibetan folk medicine, and repeated column chromatography and preparative high-performance liquid chromatography for n-butanol fraction yielded four phenylethanoid glycosides, crenatoside (1), 3 000 -O-methylcrenatoside (2), leucoseceptoside A (3), and martynoside (4). The chemical structures were identified on the basis of spectroscopic data analyses including NMR and MS. All compounds were isolated for the first time from the plant. Compound 1 exerted better 1,1-diphenyl-2-picrylhydrazyl free radical scavenging activity. In addition, compounds 1-4 were evaluated for their hepatoprotective activity on carbon tetrachloride (CCl 4 )-induced liver injury in HepG2 cells. Pretreatment of HepG2 cells with compound 1-4 significantly increased the viability on CCl 4 -induced cell death. Furthermore, compounds 1-4 also alleviated CCl 4 -induced hepatotoxicity by enhancement of the antioxidant enzyme activities of superoxide dismutase and reduction of the malondialdehyde content, intracellular ROS as well as NF-jB transactivation. Our results suggest that phenylethanoid glycosides ameliorate CCl 4 -induced cell injury, and this protection was likely due to antioxidative activity and down-regulation of NF-jB.

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Section: Effect Of Isolated Compounds On Viability Of CCL 4 -Induced mentioning

confidence: 99%

Hepatoprotective effect of phenylethanoid glycosides from Incarvillea compacta against CCl4-induced cytotoxicity in HepG2 cells

Shen

Zhang

et al. 2015

J Korean Soc Appl Biol Chem

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“…ROS, such as superoxide anion radical and hydrogen peroxide, are considered essential to enhance steroidogenesis and ovulation (Sawada & Carlson 1996, Shkolnik et al 2011. Thus, and considering that i) LH-induced ROS production seems to be an essential preovulatory signaling event by being involved in the activation of different signaling pathways (MAPK and probably PKA) (Shkolnik et al 2011); ii) leptin regulates the ovulatory process by modifying steroidogenesis ; and iii) some evidences indicate that leptin decreases ROS levels (Balasubramaniyan et al 2007) in parallel with an increase in the antioxidant defenses (Sailaja et al 2004), we hypothesize that the leptin action may affect the oxidative status, such as ROS production or antioxidant defense bioavailability, depending on its circulating levels.…”

Section: Introductionmentioning

confidence: 99%

Regulation of the ovarian oxidative status by leptin during the ovulatory process in rats

Bilbao¹,

Yorio²,

Galarza³

et al. 2015

Reproduction

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Leptin exerts both stimulatory and inhibitory effects on the ovulatory process. In this study, we investigated whether these opposite effects involve changes in the oxidative status in response to different levels of leptin. To this end, we performed both in vivo and in vitro assays using ovaries of immature rats primed with gonadotropins to induce ovulation. Superoxide dismutase (SOD) and catalase (CAT) activity, lipid peroxidation, glutathione (GSH) content, and reactive oxygen species (ROS) were studied as oxidative damage-related parameters. The expression of BCL2, BAX, and caspase 3 were measured by western blot as apoptosis-related biomarkers. The acute treatment with leptin, which inhibits ovulation, decreased SOD activity and increased active caspase 3 expression. No differences were found in CAT activity, lipid peroxidation, or total GSH. In contrast, the daily administration of leptin, which induces ovulation, decreased GSH content, ROS levels, and Bax and active caspase 3 expression, but caused no changes in other parameters. In addition, the daily administration of leptin induced follicular growth, measured by the number of antral follicles in ovarian sections. Using ovarian explant cultures, we found increased BCL2 expression and decreased SOD activity at low and high concentrations of leptin respectively. Thus, leptin can modulate the oxidative status of the ovarian tissue, during the ovulatory process, by acting on different targets according to its circulating levels. At low concentration, leptin seems to play a protective role against the oxidative stress, whereas at high concentrations, this protein seems to be involved in cell death.

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“…It is probably responsible for auto-activa tion of the normally quiescent zymogen proform of caspase-8, which further activates caspase-3, the final step in apoptotic cell death. It has been demonstrated that alco hol sensitizes primary hepatocytes and HepG2 cells to TNFα-mediated toxicity [25]. It also alters the activity of phospholipase C, phospholipase D, adenylate cyclase, PKC, JNK, p42/p44 MAPK, STAT and NFκB in hepatic tissues [27].…”

Section: Balkan Journal Of Medical Geneticsmentioning

confidence: 99%

“…Chronic ethanol-induced hepatic disease is characterized by progressive evolution from steatosis to chronic hepatitis, fibrosis, cirrhosis and HCC [25]. How ever, HCC has been iden-…”

Section: Alcohol-mediated Hepatocarc Inogenesismentioning

confidence: 99%

Molecular Pathogenesis of Hepatocellular Carcinoma

Metodieva

2007

Balkan Journal of Medical Genetics

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Metodieva SNThe most important risk factors for the development of human hepatocellular carcinoma (HCC) are chronic infec tion with hepatitis B virus (HBV) and/ or hepatitis C virus (HCV), high dietary exposure to hepatic carcinogen afla toxin B1 and alcohol abuse. Hepatitis B virus exerts its effects through integration of the viral DNA into the hepa tocyte genome, or through acting as transcriptional regu lator for several cellular proto-oncogenes and tumor-sup pressor genes. Hepatitis C virus may affect hepatocytes via the transcriptional regulation activity of the HCV core protein or via the HCV non structural proteins NS5A, NS5B and NS2, interfering with the regulation of cell cycle and apoptosis. Environmental exposure to aflatoxin B1 can cause a specific missense mutation in codon 249 of the p53 tumor-suppressor gene. Habitual alcohol consump tion leads to production of reactive oxygen species and peroxidation damage to DNA. The objective of this review is to make you acquainted with the most common risk factors and the most frequent genetic aberrations associ ated with the development of HCC.

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Mouse recombinant leptin protects human hepatoma HepG2 against apoptosis, TNF-α response and oxidative stress induced by the hepatotoxin–ethanol

Cited by 30 publications

References 42 publications

Hepatoprotective effect of phenylethanoid glycosides from Incarvillea compacta against CCl4-induced cytotoxicity in HepG2 cells

Hepatoprotective effect of phenylethanoid glycosides from Incarvillea compacta against CCl4-induced cytotoxicity in HepG2 cells

Regulation of the ovarian oxidative status by leptin during the ovulatory process in rats

Molecular Pathogenesis of Hepatocellular Carcinoma

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