Effects of curcumin on angiotensin-converting enzyme gene expression, oxidative stress and anti-oxidant status in thioacetamide-induced hepatotoxicity

Fazal, Yumna; Fatima, Syeda Nuzhat; Shahid, Syed Muhammad; Mahboob, Tabassum

doi:10.1177/1470320314545777

Cited by 35 publications

(29 citation statements)

References 25 publications

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“…These findings are in harmony with results of Ali et al, (2016) who indicated significant decreases in serum aminotransferases, and total and direct bilirubin levels in rats group given curcumin when compared to the untreated TAA intoxicated group. In another study , a significantly lower level was observed for the liver-specific enzymes(AST, ALT and ALP) in rats group treated with TAA and curcumin compared with the TAA-treated group (Fazal et al, 2014). Serum levels of transaminases return to normal may be a consequence of healing of hepatic parenchyma, stabilization of plasma membrane regeneration of hepatocytes, as well as repair of hepatic tissue damage caused by TAA (Palanivel, 2008, Vadivu et al, 2010, Moustafa et al, 2014.…”

Section: Discussionmentioning

confidence: 94%

Antioxidant Potential, Anti-Inflammatory and Hepatoprotective Effect of Curcumin in a Rat Model of Hepatotoxicity

Hussein

Ragab

Senosi

et al. 2018

Benha Veterinary Medical Journal

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Curcumin [1,7-bis (4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] was shown to exert potent antioxidant, anti-inflammatory and hepatoprotective properties. This study was done to investigate the protective effects of curcumin in thioacetamide (TAA)-induced hepatic injury in rats. Thirty-six male albino rats were divided into three equal groups. Group I (normal control group). Group II (TAA-intoxicated group): rats received thioacetamide (50 mg/kg b. wt. ip) twice weekly for 6 weeks. Group III (TAA + curcumin co-treated group): rats received thioacetamide (50 mg/kg b. wt.) and simultaneously administered curcumin (200 mg/kg b. wt./daily/orally) for 6 weeks (end of experiment). All animals were sacrificed after 6 weeks. TAA administration induced liver damage manifested by the significant increases in serum levels of ALT, AST, ALP and total bilirubin compared with control group. Oxidative stress in the group II was manifested by a significant rise in L-MDA levels with a marked reduction in the activities of antioxidant enzymes like GST, catalase CAT and depletion of GSH content in liver tissues as compared with the control group. On the other hand, TAA significantly affected the inflammation markers represented by elevation of myeloperoxidase (MPO) activities and upregulation of interleukin-6 (IL-6) gene expression levels in liver tissues. The coadministration of curcumin and thioacetamide (protection modality) prevented liver injury by normalizing the biochemical parameters, lipid peroxidation index and improving the protein oxidation, inflammatory markers and the antioxidant status. These findings suggested that, liver injury could be curtailed by the antioxidant and anti-inflammatory activities of curcumin and the normal status of the liver could be preserved.

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Section: Discussionmentioning

confidence: 94%

Antioxidant Potential, Anti-Inflammatory and Hepatoprotective Effect of Curcumin in a Rat Model of Hepatotoxicity

Hussein

Ragab

Senosi

et al. 2018

Benha Veterinary Medical Journal

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“…CURa natural compoundhas attracted more and more attention for as an anti-oxidant. Results from Fazal et al 28 .…”

Section: Discussionmentioning

confidence: 95%

“…CUR – a natural compound – has attracted more and more attention for as an anti‐oxidant. Results from Fazal et al . showed that CUR could reduce oxidative stress in animals by scavenging ROS, protect the anti‐oxidant enzymes from being denatured and reduce the oxidative stress marker lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Curcumin attenuates high glucose‐induced inflammatory injury through the reactive oxygen species–phosphoinositide 3‐kinase/protein kinase B–nuclear factor‐κB signaling pathway in rat thoracic aorta endothelial cells

Zhang

2017

J of Diabetes Invest

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Aims/IntroductionEndothelial cell inflammatory injury is likely required for barrier dysfunction under hyperglycemic conditions. Curcumin (CUR) is well known for its anti‐inflammatory effect. However, there have been few reports about the anti‐inflammatory effect of CUR induced by high glucose in endothelial cells. The aim of the present study was to investigate the inflammatory effect of high glucose and the anti‐inflammatory effect of CUR induced by high glucose in rat thoracic aorta endothelial cells (TAECs).Materials and MethodsWell characterized TAECs were established and cell viability was assayed by the cell counting kit‐8 method, messenger ribonucleic acid and protein expression were identified by real‐time polymerase chain reaction, western blot or enzyme‐linked immunosorbent assay, respectively. The production of reactive oxygen species was observed by a fluorescence microscope.ResultsHigh glucose (30 mmol/L) significantly decreased the cell viability of TAECs after being co‐cultivated for 12 h and showed a time‐dependent manner, and increased interleukin (IL)‐1β, IL‐6 and tumor necrosis factor‐α secretion in TAECs. The injury effect of high glucose was involved in the reactive oxygen species–phosphoinositide 3‐kinase (PI3K)/protein kinase B (AKT)–nuclear factor (NF)‐κB signaling pathway. Anti‐oxidant N‐acetylcysteine, PI3K and NF‐κB‐specific pathway inhibitors can abolish the secretion of these inflammatory factors; pretreatment with anti‐oxidant N‐acetylcysteine significantly decreased PI3K expression, the level of phosphorylated AKT and nuclear NF‐κB; pretreatment of LY294002 can significantly decrease the NF‐κB level in nuclei. After treatment with CUR for 12 h, IL‐1β, IL‐6 and tumor necrosis factor‐α secretion were markedly decreased, and PI3K expression, the phosphorylation of AKT and nuclear NF‐κB level were also decreased.ConclusionCurcumin attenuates high glucose‐induced inflammatory injury through the reactive oxygen species–PI3K/AKT–NF‐κB signaling pathway in rat thoracic aorta endothelial cells.

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“…The TAA-induced hepatic injury and HE have been established in many studies biochemically and histologically with increased blood ammonia levels (Zimmermann et al 1989;Abdel-hameed et al 2014;Stefanello et al 2015 andLebda et al 2018). They reported oxidative damage in liver and brain tissues indicated by increased intracellular reactive oxygen species (ROS) production (Bruck et al 2004;Fazal et al 2015 andStefanello et al 2015). These "ROS" interfere with energy utilization by exerting toxic effects on the liver mitochondria (Chu et al 2001) and bind covalently to liver macromolecules leading to leakage of destructive hydrolytic proteases as calpains from dying cells (Chilakapati et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Hibiscus Sabdariffa Aqueous Extract Ameliorates Thioacetamide-Induced Hepatic Encephalopathy in Guinea Pigs: Role of Ammonia Extraction

Alalkam

2018

Al-Azhar Journal of Pharmaceutical Sciences

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The current work assessed the preventive and therapeutic potential of Hibiscus sabdariffa "HS" aqueous extract (HSE) on thioacetamide (TAA)-induced hepatic encephalopathy (HE) associated with the acute liver injury. Method: guinea pigs were divided into: Group 1 (Control group n=24) which was further subdivided into 4 subgroups; Group "1-a" (non-treated); Group "1-b" given HSE for 3 days and sacrificed on the 4 th day; Group "1-c" given TAA for 3 days and sacrificed on the 4 th day; Group "1d" given the TAA doses for 3 days and sacrificed on the 7 th day; Group 2 (Preventive) given TAA and HSE doses concurrently for 3 days and sacrificed on the 4 th day. Group 3 (Therapeutic) given 3-days TAA followed by 3-days HSE doses and sacrificed on the 7 th day. Results: Preventive and therapeutic HSE resulted in significant amelioration of the TAA-induced hepatic encephalopathy with faster recovery of animals on the 7 th day associated with significant improvement in the biochemical parameters of liver injury including the ammonia extraction ratio indicating functional hepatic improvement. In addition, there was a significant improvement in brain edema. Conclusion: HSE has both preventive and therapeutic effects on TAA-induced hepatic encephalopathy and liver injury in guinea pigs

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Effects of curcumin on angiotensin-converting enzyme gene expression, oxidative stress and anti-oxidant status in thioacetamide-induced hepatotoxicity

Cited by 35 publications

References 25 publications

Antioxidant Potential, Anti-Inflammatory and Hepatoprotective Effect of Curcumin in a Rat Model of Hepatotoxicity

Antioxidant Potential, Anti-Inflammatory and Hepatoprotective Effect of Curcumin in a Rat Model of Hepatotoxicity

Curcumin attenuates high glucose‐induced inflammatory injury through the reactive oxygen species–phosphoinositide 3‐kinase/protein kinase B–nuclear factor‐κB signaling pathway in rat thoracic aorta endothelial cells

Hibiscus Sabdariffa Aqueous Extract Ameliorates Thioacetamide-Induced Hepatic Encephalopathy in Guinea Pigs: Role of Ammonia Extraction

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