Supplementation of curcumin and vitamin E enhances oxidative stress, but restores hepatic histoarchitecture in hypothyroid rats

Subudhi, Umakanta; Das, Kajari; Paital, Biswaranjan; Bhanja, Shravani; Chainy, G.B.N.

doi:10.1016/j.lfs.2008.12.024

Cited by 61 publications

(35 citation statements)

References 45 publications

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“…They protect DNA against oxidative attack, thereby lowering the risk for mutations and other genetic damage (Hatcher et al, 2008;Garcea et al, 2005). They also activate detoxification enzymes such as glutathione S-transferase (Subudhi et al, 2009). Curcumins can down-regulate NF-κB, a nuclear transcription factor and critical upstream regulator of genes that control acute and chronic inflammation cascades (Singh and Aggarwal, 1995;Sarkar et al, 2008).…”

Section: Stress Parametersmentioning

confidence: 99%

Evaluation of Protective Potential of Curcuma longa in Induced Aflatoxicosis in Broiler Birds

Raja¹,

Singh²,

Mondal³

et al. 2017

Int.J.Curr.Microbiol.App.Sci

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Section: Stress Parametersmentioning

confidence: 99%

Evaluation of Protective Potential of Curcuma longa in Induced Aflatoxicosis in Broiler Birds

Raja¹,

Singh²,

Mondal³

et al. 2017

Int.J.Curr.Microbiol.App.Sci

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“…[27][28][29][30] Samples from liver were separated and fixed, and then embedded and stained with hematoxylin and eosin. Each index was calculated using automated image analysis (DMI-300 Image Processing; DMI, Korea).…”

Section: )mentioning

confidence: 99%

“…27,30) In addition, total hepatocyte numbers were also calculated according to previous established methods. 28,29) Statistical Analysis For each treatment showing a statistically significant effect, the Student's t-test analysis was used for comparisons of group means.…”

Section: )mentioning

confidence: 99%

Tacrine, an Oral Acetylcholinesterase Inhibitor, Induced Hepatic Oxidative Damage, Which Was Blocked by Liquiritigenin through GSK3-beta Inhibition

Park

Han

et al. 2015

Biological & Pharmaceutical Bulletin

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Although the cholinesterase inhibitor tacrine has been successfully used for the treatment of Alzheimer's disease, it is known to have hepatotoxic effects. Liquiritigenin (LQ), an active flavonoid in Glycyrrhizae radix, exerts protective effects against liver damage. This study investigated the toxic effect of tacrine on hepatocytes and the beneficial effect of LQ on tacrine intoxication in vivo and in vitro, and the underlying mechanism involved. In hepatocyte cell lines, tacrine induced cell death and oxidative stress, as indicated by decreases in cell viability and glutathione (GSH) contents, which were blocked by pretreatment with LQ. Fluorescent activated cell sorter (FACS) analysis revealed that LQ inhibited cellular H 2 O 2 production and mitochondrial dysfunction induced by tacrine in HepG2 cells. Furthermore, LQ promoted inhibitory phosphorylation of glycogen synthase kinase-3β (GSK3β) and prevented decreases in GSK3β phosphorylation induced by tacrine. In rats treatment with tacrine at 30 mg/kg increased hepatic damage as assessed by blood biochemistry and histopathology. Administration of LQ (10 or 30 mg/kg/d, per os (p.o.)) or the hepatoprotective drug sylimarin (100 mg/kg/d) for 3 d inhibited elevations in alanine aminotransferase, aspartate aminotransferase, and histological changes induced by tacrine. These results show that LQ efficaciously protects the rat liver against tacrine-induced liver damage, and suggest that LQ is a therapeutic candidate for ameliorating the hepatotoxic effects of tacrine.Key words tacrine; liquiritigenin; glycogen synthase kinase-3β; liver; oxidative stress; mitochondria Tacrine (9-amino-1,2,3,4-tetrahydroacridine hydrochloride) is recommended as the first-line treatment for Alzheimer's disease by the US Food and Drug Administration. It is an active cholinesterase inhibitor that blocks the degradation of cholinergic nerves in the cerebral cortex and hippocampus to increase cholinergic transmission. 1) However, although tacrine has positive therapeutic effects, it has been demonstrated to increased serum alanine aminotransferase (ALT) levels in about 30% of patients, and this seriously limits its clinical use.2) A number of authors have reported that tacrine-induced hepatotoxicity is related to cytochrome P450 1A2 in human liver microsomes and is associated with mitochondrial dysfunction.3-5) Studies also have showed that the hepatotoxic effect of tacrine is associated with oxidative stress, as demonstrated by increased reactive oxygen species (ROS) production and decreased intracellular glutathione (GSH).6-8) However, mechanism responsible for tacrine-induced hepatotoxicity has not yet been elucidated. Nevertheless many studies have shown that anthraquinones, chromone glycosides, phenolic amide, and an herbal medicine protect hepatocytes from the toxic effects of tacrine. [9][10][11][12] Oxidative stress is state in which the balance between ROS production and antioxidants is shifted in favor of ROS, and is associated with severity of liver damage.13) ROS normally work ...

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“…The naturally occurring Curcuma longa (turmeric) have major phenolic compound curcumin which is a powerful immunomodulatory agent which has anti-inflammatory, antioxidant, anti-cancerous, anti-amyloid and food preservative properties (26)(27)(28). The curcumin 1 to 5 gm/kg of body weight do not cause any adverse effect (29) and long-term administration of curcumin to rodents leads to hyperproliferation of thyroid epithelial cells (30).…”

Section: Introductionmentioning

confidence: 99%

The Efficiency of Mitochondria-Targeted Curcumin in Reducing Thyroid Mitochondrial Oxidative Damage

2017

IJSR

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Mitochondria are the crucial site for the cellular energy production. The antioxidant has less therapeutic success to overcome mitochondrial toxicity produced by oxidative stress due to mitochondrial inability in accepting antioxidant. In the present investigation, we synthesized selective mitochondrial targeted curcumin for easy transport to mitochondria of the thyroid gland. Our observation shows the strong antioxidant effect of mitochondrial targeted curcumin against lipid peroxidation and mitochondrial transition induced by Escherichia coli. Mitochondria-targeted curcumin significantly improved endogenous glutathione level in the mitochondria, its protect the motochondrial defense system against oxidative damage. Thus it is concluded that mitochondria-targeted curcumin protects mitochondria against E.coli toxicity of thyroid gland, By lowering the oxidative damage, increasing the level of reduced glutathione and preserving the mitochondrial integrity.

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Supplementation of curcumin and vitamin E enhances oxidative stress, but restores hepatic histoarchitecture in hypothyroid rats

Cited by 61 publications

References 45 publications

Evaluation of Protective Potential of Curcuma longa in Induced Aflatoxicosis in Broiler Birds

Evaluation of Protective Potential of Curcuma longa in Induced Aflatoxicosis in Broiler Birds

Tacrine, an Oral Acetylcholinesterase Inhibitor, Induced Hepatic Oxidative Damage, Which Was Blocked by Liquiritigenin through GSK3-beta Inhibition

The Efficiency of Mitochondria-Targeted Curcumin in Reducing Thyroid Mitochondrial Oxidative Damage

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