Molecular hepatoprotective effects of lipoic acid against carbon tetrachloride-induced liver fibrosis in rats

Sadek, Kadry M.; Saleh, EA; Nasr, Sherif

doi:10.1177/0960327117693066

Cited by 37 publications

(20 citation statements)

References 41 publications

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“…Moreover, β-arrestin-2 takes an interest in the Wnt flagging pathway (Bryja et al 2007), which is as often as possible imbalanced in hepatocarcinoma. The expanded generation of ROS is a mechanism by which certain exogenous chemicals instigate apoptosis; along these lines, chemicals that actuate antioxidation produce hostile to apoptotic impacts (Sadek et al 2017a). In addition, certain chemicals forestall tumor by upgrading antioxidant impact and inciting cell death.…”

Section: Discussionmentioning

confidence: 99%

Role and potential targeting of hepatic apurinic/apyrimidinic endonuclease-1 and cyclin-dependent kinase-4 in hepatocellular carcinoma

2018

Can. J. Physiol. Pharmacol.

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Section: Discussionmentioning

confidence: 99%

Role and potential targeting of hepatic apurinic/apyrimidinic endonuclease-1 and cyclin-dependent kinase-4 in hepatocellular carcinoma

2018

Can. J. Physiol. Pharmacol.

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“…In a rat model of bile duct ligation (BDL)-induced liver fibrosis ALA downregulated the hepatic inhibitor-1 of the plasminogen activator inhibitor-1 (PAI-1) expression by inhibiting the TGF-β signaling mediators, like Smad3, activator protein-1 (AP1), and specificity protein 1 (Sp1) [51]. Yet, in a CCl 4 -induced liver fibrosis model ALA prevented collagen deposition and oxidative stress, as well as it modulated the expression of the pro-inflammatory cytokine interleukin-6 (IL-6), the inducible nitric oxyde synthase (iNOS), the NF-kB, and the MMP-13 [52]. ALA also provided protection from liver ischemia-reperfusion injury [53] or from tissue damage induced with different treatments, including lipopolysaccharide/D-galactosamine/methotrexate injection [54,55,56,57,58,59], bisphenol-A oral administration [60], a high fat or fructose rich diet [61,62,63] or methionine–choline deficiency [64].…”

Section: Natural Sulfur-containing Compounds For the Treatment Ofmentioning

confidence: 99%

Natural Sulfur-Containing Compounds: An Alternative Therapeutic Strategy against Liver Fibrosis

Milito

Brancaccio

D’Argenio

et al. 2019

Cells

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Liver fibrosis is a pathophysiologic process involving the accumulation of extracellular matrix proteins as collagen deposition. Advanced liver fibrosis can evolve in cirrhosis, portal hypertension and often requires liver transplantation. At the cellular level, hepatic fibrosis involves the activation of hepatic stellate cells and their transdifferentiation into myofibroblasts. Numerous pro-fibrogenic mediators including the transforming growth factor-β1, the platelet-derived growth factor, endothelin-1, toll-like receptor 4, and reactive oxygen species are key players in this process. Knowledge of the cellular and molecular mechanisms underlying hepatic fibrosis development need to be extended to find novel therapeutic strategies. Antifibrotic therapies aim to inhibit the accumulation of fibrogenic cells and/or prevent the deposition of extracellular matrix proteins. Natural products from terrestrial and marine sources, including sulfur-containing compounds, exhibit promising activities for the treatment of fibrotic pathology. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans are largely unknown. This review aims to provide a reference collection on experimentally tested natural anti-fibrotic compounds, with particular attention on sulfur-containing molecules. Their chemical structure, sources, mode of action, molecular targets, and pharmacological activity in the treatment of liver disease will be discussed.

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“…Drug-induced liver damage is responsible for 5% of all hospital admissions and 50% of patients suffered with acute liver failure [ 1 ]. It is known that carbon tetrachloride (CCl 4 ) causes liver damage and hepatocyte apoptosis/necrosis in vitro and in vivo [ 2 , 3 , 4 , 5 ]. Liver damage from CCl 4 is a common model used to measure the efficiency of many hepatoprotective drugs [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…Then, these radicals attack cellular macromolecules and cause lipid peroxidation, protein degradation, and DNA damage. The process is followed by the release of hepatic inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), which leads to eventual damage, including hepatocellular necrosis [ 2 , 4 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Hepatoprotective Effects of Four Endemic Cirsium Species Extracts from Taiwan on CCl4-Induced Acute Liver Damage in C57BL/6 Mice

Zhao

Chang

Lin

et al. 2018

IJMS

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Species of Cirsium (Asteraceae family) have been used in folk hepatoprotective medicine in Taiwan. We collected four Cirsium species—including the aerial part of Cirsium arisanense (CAH), the aerial part of Cirsium kawakamii (CKH), the flower part of Cirsium japonicum DC. var. australe (CJF), and Cirsii Herba (CH)—and then made extractions from them with 70% methanol. We compared the antioxidant contents and activities of these four Cirsium species extracts by a spectrophotometric method and high-performance liquid chromatography–photodiode array detector (HPLC-DAD). We further evaluated the hepatoprotective effects of these extracts on CCl4-induced acute liver damage in C57BL/6 mice. The present study found CAH possesses the highest antioxidant activity among the four Cirsium species, and these antioxidant activities are closely related to phenylpropanoid glycoside (PPG) contents. The extracts decreased serum ALT and AST levels elevated by injection with 0.2% CCl4. However, only CJF and CH decreased hepatic necrosis. Silibinin decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and hepatic necrosis caused by CCl4. CJF and CH restored the activities of hepatic antioxidant enzymes and decreased hepatic malondialdehyde (MDA) levels. CJF further restored the expression of hepatic antioxidant enzymes including Cu/Zn-superoxide dismutase (Cu/Zn-SOD), Mn-superoxide dismutase (Mn-SOD), and glutathione S-transferase (GST) proteins. HPLC chromatogram indicated that CKH, CJF, and CH contained silibinin diastereomers (α and β). Only CJF contained diosmetin. Hence, the hepatoprotective mechanism of CJF against CCl4-induced acute liver damage might be involved in restoring the activities and protein expression of the hepatic antioxidant defense system and inhibiting hepatic inflammation, and these hepatoprotective effects are related to the contents of silibinin diastereomers and diosmetin.

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Molecular hepatoprotective effects of lipoic acid against carbon tetrachloride-induced liver fibrosis in rats

Abstract: These outcomes show that α-LA might be compelling at forestalling collagen deposition and hepatic oxidative stress as well as downregulating the expression of hepatic proinflammatory cytokines, iNOS, and NF-κB and upregulating MMP-13 expression.

Cited by 37 publications

References 41 publications

Role and potential targeting of hepatic apurinic/apyrimidinic endonuclease-1 and cyclin-dependent kinase-4 in hepatocellular carcinoma

Role and potential targeting of hepatic apurinic/apyrimidinic endonuclease-1 and cyclin-dependent kinase-4 in hepatocellular carcinoma

Natural Sulfur-Containing Compounds: An Alternative Therapeutic Strategy against Liver Fibrosis

Comparison of the Hepatoprotective Effects of Four Endemic Cirsium Species Extracts from Taiwan on CCl4-Induced Acute Liver Damage in C57BL/6 Mice

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