rebaudioside-a has been researched along with Chemical-and-Drug-Induced-Liver-Injury* in 2 studies
2 other study(ies) available for rebaudioside-a and Chemical-and-Drug-Induced-Liver-Injury
| Article | Year |
|---|---|
Stevia Prevents Acute and Chronic Liver Injury Induced by Carbon Tetrachloride by Blocking Oxidative Stress through Nrf2 Upregulation.
The effect of stevia on liver cirrhosis has not been previously investigated. In the present study, the antioxidant and anti-inflammatory properties of stevia leaves were studied in male Wistar rats with carbon tetrachloride- (CCl Topics: Animals; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Chemical and Drug Induced Liver Injury, Chronic; Humans; Liver; Liver Cirrhosis; Male; NF-E2-Related Factor 2; Oxidative Stress; Pilot Projects; Rats; Rats, Wistar; Stevia; Up-Regulation | 2018 |
Stevia and stevioside protect against cisplatin nephrotoxicity through inhibition of ERK1/2, STAT3, and NF-κB activation.
We investigated the effect of natural sweetener Stevia rebaudiana and its constituent stevioside in cisplatin (CP)-induced kidney injury. Male BALB/cN mice were orally administered 10, 20, and 50 mg/kg body weight of Stevia rebaudiana ethanol extract (SE) or stevioside 50 mg/kg, 48 h after intraperitoneal administration of CP (13 mg/kg). Two days later, CP treatment resulted in histopathological changes showing kidney injury. Increased expression of 4-hydroxynonenal (4-HNE), 3-nitrotyrosine (3-NT), and heme oxygenase-1 (HO-1) in mice kidneys suggested oxidative stress. CP treatment also increased renal expression of nuclear factor-kappaB (NF-κB) p65 subunit and phosphorylated inhibitor of NF-κB (IκBα), as well as expression of pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α). Induction of apoptosis and inhibition of the cell cycle in kidneys was evidenced by increased expression of p53, Bax, caspase-9, and p21, proteolytic cleavage of poly (ADP-ribose) polymerase (PARP), with concomitant suppression of Bcl-2 and cyclin D1 expression. The number of apoptotic cells in kidneys was also assessed. CP administration resulted in activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and signal transducer and activator of transcription 3 (STAT3). Both SE and stevioside attenuated CP nephrotoxicity by suppressing oxidative stress, inflammation, and apoptosis through mechanism involving ERK1/2, STAT3, and NF-κB suppression. Topics: Animals; Antineoplastic Agents; Apoptosis; Caspase 9; Chemical and Drug Induced Liver Injury; Cisplatin; Diterpenes, Kaurane; Glucosides; Heme Oxygenase-1; Humans; Kidney; Male; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinase 3; NF-kappa B; Oxidative Stress; Poly(ADP-ribose) Polymerases; Protective Agents; Stevia; Tumor Necrosis Factor-alpha | 2017 |