Silymarin and caffeine combination ameliorates experimentally-induced hepatic fibrosis through down-regulation of LPAR1 expression

Eraky, Salma M.; El-Mesery, Mohamed; El-Karef, Amro; Eissa, Laila A.; El-Gayar, Amal M.

doi:10.1016/j.biopha.2018.02.064

Cited by 35 publications

(28 citation statements)

References 56 publications

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“…The degree of protection was maximally observed in silymarin (50 mg/kg bw/p.o)-treated groups when compared with J. tranquebariensis (400 mg/kg bw). This degree of hepatoprotection could be based on its various properties of anti-oxidation, inhibition of lipid peroxidation, regeneration of intracellular glutathione content, protein synthesis and improvement of liver regeneration from hepatocellular necrosis [ 37 , 38 , 39 , 40 , 41 , 42 , 43 ]. Furthermore, it stabilizes cellular membranes and regulates membrane permeability that inhibits toxins entry into liver cells.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Aqueous Extract from the Leaves of Justicia tranquebariesis against Thioacetamide-Induced Oxidative Stress and Hepatic Fibrosis in Rats

Sukalingam

Ganesan

2018

Antioxidants

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The present study aims to examine the protective effect of Justicia tranquebariesis on thioacetamide (TAA)-induced oxidative stress and hepatic fibrosis. Male Wister albino rats (150–200 g) were divided into five groups. Group 1 was normal control. Group 2 was J. tranquebariensis (400 mg/kg bw/p.o.)-treated control. Group 3 was TAA (100 mg/kg bw/s.c.)-treated control. Groups 4 and 5 were orally administered with the leaf extract of J. tranquebariensis (400 mg/kg bw) and silymarin (50 mg/kg bw) daily for 10 days with a subsequent administration of a single dose of TAA (100 mg/kg/s.c.). Blood and livers were collected and assayed for various antioxidant enzymes (SOD, CAT, GPx, GST, GSH, and GR). Treatment with J. tranquebariensis significantly reduced liver TBARS and enhanced the activities of antioxidant enzymes in TAA-induced fibrosis rats. Concurrently, pretreatment with J. tranquebariensis significantly reduced the elevated liver markers (AST, ALT, ALP, GGT, and TB) in the blood. In addition, J. tranquebariensis- and silymarin- administered rats demonstrated the restoration of normal liver histology and reduction in fibronectin and collagen deposition. Based on these findings, J. tranquebariensis has potent liver protective functions and can alleviate thioacetamide-induced oxidative stress, hepatic fibrosis and possible engross mechanisms connected to antioxidant potential.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Aqueous Extract from the Leaves of Justicia tranquebariesis against Thioacetamide-Induced Oxidative Stress and Hepatic Fibrosis in Rats

Sukalingam

Ganesan

2018

Antioxidants

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“…10 Besides the normal control (NC) group receiving the vehicle, 5 groups of rats (n ¼ 8) were given freshly prepared thioacetamide (TAA) (200 mg/kg, intraperitoneally) twice weekly for 8 weeks. [11][12][13] The 5 TAA groups included a positive control group (PC, untreated) and 4 treated groups orally for another 2 months as follows: the first and second groups received telmisartan standard drug low & high doses (TL & TH: 1.8 and 3.6 mg/kg/day) while the third and fourth groups received telmisartan SNEDDS at the same low and high doses (TLS & THS). 9,14,15 Then blood samples were obtained and then rats were sacrificed.…”

Section: In Vivo Studymentioning

confidence: 99%

Telmisartan Self-Nanoemulsifying Drug Delivery System, Compared With Standard Telmisartan, More Effectively Improves Hepatic Fibrosis in Rats

et al. 2020

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Background: This study was designed to examine effects of telmisartan; an angiotensin receptor blocker; self-nanoemulsifying drug delivery system (SNEDDS) in reversing already-established hepatic fibrosis. Method: Forty rats were given thioacetamide (200 mg/kg, intraperitoneally) twice/week for 8 weeks then divided into 5 groups (n = 8), PC and 4 treated groups. Treatments were given orally for another 2 months as follows: telmisartan low and high doses (TL and TH: 1.8 and 3.6 mg/kg/day) and telmisartan SNEDDS at the same doses (TLS and THS). At end of treatment, blood was obtained and liver was isolated. Results: Rats showed significant elevations of plasma ALT and AST and hepatic IL-6, TNF-α, and MDA, significant reductions of plasma albumin, hepatic GSH, and body weight, and hepatic histopathological damage. All treatments except for TL significantly reversed these thioacetamide-induced changes. THS group showed significant differences from all groups. Regarding ratio of free telmisartan concentration in hepatic homogenate to that of plasma, TH and TLS groups showed non-significant variation between each other while THS group showed significant differences from them. No significant changes were detected in blood pressure, hemoglobin, white blood cells, and platelets. Conclusion: Telmisartan SNEDDS, compared with telmisartan, more effectively reversed chronic hepatic fibrosis with good safety profile.

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“…Later, all studies confirmed the antifibrotic properties of caffeine as assessed by histology or liver biochemistry. [79][80][81][82][83][84][85][86][87][88] Most studies explained this by the inhibition of TGFβ and the subsequent decreased αSMA and CTGF expression upon caffeine treatment. [81][82][83]87,88 Also, caffeine decreased MDA (i.e., lipid peroxidation) and increased superoxidase dismutase and glutathione concentration.…”

Section: Fibrosismentioning

confidence: 99%

“…[79][80][81][82][83][84][85][86][87][88] Most studies explained this by the inhibition of TGFβ and the subsequent decreased αSMA and CTGF expression upon caffeine treatment. [81][82][83]87,88 Also, caffeine decreased MDA (i.e., lipid peroxidation) and increased superoxidase dismutase and glutathione concentration. 81,83,[85][86][87] Gordillo-Bastidas et al treated rats with either bile duct ligation or TAA and discovered that caffeine decreased transcriptional factor Snail-1 (important in the activation of HSCs) and increased Nrf2.…”

Section: Fibrosismentioning

confidence: 99%

Potential Mechanisms Underlying the Role of Coffee in Liver Health

2018

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Coffee, the most consumed hot beverage worldwide, is composed of many substances, of which polyphenols, caffeine, and diterpenoids are well studied. Evidence on potential effects of coffee on human health has been accumulating over the past decades. Specifically, coffee has been postulated to be hepatoprotective in several epidemiological and clinical studies. Several underlying molecular mechanisms as to why coffee influences liver health have been proposed. In this review, the authors summarized the evidence on potential mechanisms by which coffee affects liver steatosis, fibrosis, and hepatic carcinogenesis. The experimental models reviewed almost unanimously supported the theorem that coffee indeed may benefit the liver. Either whole coffee or its specific compounds appeared to decrease fatty acid synthesis (involved in steatogenesis), hepatic stellate activation (involved in fibrogenesis), and hepatic inflammation. Moreover, coffee was found to induce apoptosis and increased hepatic antioxidant capacity, which are involved in carcinogenesis.

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Silymarin and caffeine combination ameliorates experimentally-induced hepatic fibrosis through down-regulation of LPAR1 expression

Cited by 35 publications

References 56 publications

Protective Effect of Aqueous Extract from the Leaves of Justicia tranquebariesis against Thioacetamide-Induced Oxidative Stress and Hepatic Fibrosis in Rats

Protective Effect of Aqueous Extract from the Leaves of Justicia tranquebariesis against Thioacetamide-Induced Oxidative Stress and Hepatic Fibrosis in Rats

Telmisartan Self-Nanoemulsifying Drug Delivery System, Compared With Standard Telmisartan, More Effectively Improves Hepatic Fibrosis in Rats

Potential Mechanisms Underlying the Role of Coffee in Liver Health

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