scholarly journals Evaluation of redox status and organ protective effects of Aspalathus linearis extract in Arsenic exposed Rats

2021 ◽  
pp. 100171
Author(s):  
Akinboro Adetayo ◽  
Adedosu Olaniyi Temitope ◽  
Badmus Jelili Abiodun ◽  
Adegbola Peter Ifeoluwa ◽  
Abubakar Mohammed Y ◽  
...  
2013 ◽  
Vol 2013 ◽  
pp. 1-19 ◽  
Author(s):  
Olawale R. Ajuwon ◽  
Emma Katengua-Thamahane ◽  
Jacques Van Rooyen ◽  
Oluwafemi O. Oguntibeju ◽  
Jeanine L. Marnewick

The possible protective effects of an aqueous rooibos extract (Aspalathus linearis), red palm oil (RPO) (Elaeis guineensis), or their combination ontert-butyl-hydroperoxide-(t-BHP-)induced oxidative hepatotoxicity in Wistar rats were investigated.tert-butyl hydroperoxide caused a significant (P<0.05) elevation in conjugated dienes (CD) and malondialdehyde (MDA) levels, significantly (P<0.05) decreased reduced glutathione (GSH) and GSH : GSSG ratio, and induced varying changes in activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase in the blood and liver. This apparent oxidative injury was associated with histopathological changes in liver architecture and elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). Supplementation with rooibos, RPO, or their combination significantly (P<0.05) decreased CD and MDA levels in the liver and reduced serum level of ALT, AST, and LDH. Likewise, changes observed in the activities of antioxidant enzymes and impairment in redox status in the erythrocytes and liver were reversed. The observed protective effects when rooibos and RPO were supplemented concomitantly were neither additive nor synergistic. Our results suggested that rooibos and RPO, either supplemented alone or combined, are capable of alleviatingt-BHP-induced oxidative hepatotoxicity, and the mechanism of this protection may involve inhibition of lipid peroxidation and modulation of antioxidants enzymes and glutathione status.


2017 ◽  
Vol 8 (12) ◽  
pp. 4657-4667 ◽  
Author(s):  
Ge Song ◽  
Zhigang Liu ◽  
Luanfeng Wang ◽  
Renjie Shi ◽  
Chuanqi Chu ◽  
...  

Lipoic acid (LA) suppressed acrylamide (ACR)-induced inflammation, redox status disturbance, autophagy, and apoptosis mediated by mitochondria in the SH-SY5Y cells.


2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Oluwatosin Adekunle Adaramoye ◽  
Olubukola Oyebimpe Akanni

We investigated the effects of methanol extract ofArtocarpus altilis(AA) on atherogenic indices and redox status of cellular system of rats fed with dietary cholesterol while Questran (QUE) served as standard. Biochemical indices such as total cholesterol (TC), triglycerides (TG), low- and high-density lipoproteins-cholesterol (LDL-C and HDL-C), aspartate and alanine aminotransferases (AST and ALT), lactate dehydrogenase (LDH), reduced glutathione, glutathione-s-transferase, glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and lipid peroxidation (LPO) were assessed. Hypercholesterolemic (HC) rats had significantly increased relative weight of liver and heart. Dietary cholesterol caused a significant increase (P<0.05) in the levels of serum, hepatic, and cardiac TC by 110%, 70%, and 85%, LDL-C by 79%, 82%, and 176%, and TG by 68%, 96%, and 62%, respectively. Treatment with AA significantly reduced the relative weight of the organs and lipid parameters. There were beneficial increases in serum and cardiac HDL-C levels in HC rats treated with AA. In HC rats, serum LDH, ALT, and AST activities and levels of LPO were increased, whereas hepatic and cardiac SOD, CAT, and GPx were reduced. All biochemical and histological alterations were ameliorated upon treatment with AA. Extract of AA had protective effects against dietary cholesterol-induced hypercholesterolemia.


2018 ◽  
Vol 70 (6) ◽  
pp. 1195-1201 ◽  
Author(s):  
Sumin Yang ◽  
Changhun Lee ◽  
Bong-Seon Lee ◽  
Eui Kyun Park ◽  
Kyung-Min Kim ◽  
...  

2020 ◽  
Author(s):  
Abazar Ghorbani ◽  
Leila Pishkar ◽  
Nasim Roudbari ◽  
Necla Pehlivan ◽  
Chu Wu

Abstract Background: Plants do not always have the genetic capacity to tolerate high quantities of (As) which does not only arrest the plant growth, but commit potential health risks by dietary bioaccumulation. However, the interplay between the tomato plants and As-NO driven molecular cell dynamics are obscure. Hence, seedlings were treated with As (10 mg/L) alone or in combination with 100 µM sodium nitroprusside (SNP, NO donor) and 200 µM 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO, NO scavenger).Results: SNP immobilized the As in the roots and reduced the shoot translocation by up-regulating the transcriptional expression of the PCS, GSH1, MT2 and ABC1. SNP further restored the growth retardation by modulating the chlorophyll and proline metabolism, increasing NO accumulation and stomatal conductance along with a clear crosstalk between the activity of antioxidants as well as glyoxalase I and II leading endogenous H2O2 and MG decrease.Conclusion: Higher PCs and glutathione accumulation helped to protect photosynthetic apparatus, however, cPTIO reversed the protective effects of SNP, authenticating the role of NO in the As toxicity alleviation.


2018 ◽  
Vol 24 (25) ◽  
pp. 2986-2992 ◽  
Author(s):  
Xian-Si Zeng ◽  
Wen-Shuo Geng ◽  
Lei Chen ◽  
Jin-Jing Jia

Background: Cerebral ischemia is a common cause of disability and death. Ischemic brain injury results from complex pathological processes, including oxidative stress, inflammation, and apoptosis. Thioredoxin( Trx) is an important multifunctional protein, which regulates cellular redox status. Increasing studies have demonstrated that Trx provides a neuroprotective role against cerebral ischemia-induced injury. Methods: A systematic search of PMC and the PubMed Database was conducted to summarize the protective effects of Trx against cerebral ischemia. Results: This article reviews the understanding of potential effects and mechanisms of Trx against cerebral ischemia, including the anti-oxidant, anti-apoptotic and anti-inflammatory effects, as well as the activation of prosurvival pathway. We also summarize that some natural compounds induce the expression of Trx, which is involved in their anti-ischemic effects. Conclusion: In conclusion, Trx has a potential neuroprotection in cerebral ischemia and may be very promising for clinical therapy of ischemic stroke in the future.


2012 ◽  
Vol 90 (10) ◽  
pp. 1345-1353 ◽  
Author(s):  
Upa Kukongviriyapan ◽  
Kwanjit Sompamit ◽  
Patchareewan Pannangpetch ◽  
Veerapol Kukongviriyapan ◽  
Wanida Donpunha

Quercetin, a dietary antioxidant flavonoid, possesses strong anti-inflammatory and cytoprotective activities. The effects were investigated in an animal model of lipopolysaccharide (LPS)-induced endotoxaemia and vascular dysfunction in vivo. Male ICR mice were injected with LPS (10 mg/kg; i.p.). Quercetin (50 or 100 mg/kg) was intragastrically administered either before or after LPS administration. Fifteen hours after LPS injection, mice were found in endotoxaemic condition, as manifested by hypotension, tachycardia, and blunted vascular responses to vasodilators and vasoconstrictor. The symptoms were accompanied by increased aortic iNOS protein expression, decreased aortic eNOS protein expression, marked suppression of cellular glutathione (GSH) redox status, enhanced aortic superoxide production, increased plasma malodialdehyde and protein carbonyl, and elevated urinary nitrate/nitrite. Treatment with quercetin either before or after LPS preserved the vascular function, as blood pressure, heart rate, vascular responsiveness were restored to near normal values, particularly when quercetin was given as a preventive regimen. The vascular protective effects were associated with upregulation of eNOS expression, reduction of oxidative stress, and maintained blood GSH redox ratio. Overall findings suggest the beneficial effect of quercetin on the prevention and restoration of a failing eNOS system and alleviation of oxidative stress and vascular dysfunction against endotoxin-induced shock in mice.


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