Protective effects of Pycnogenol® on carbon tetrachloride-induced hepatotoxicity in Sprague–Dawley rats

Pine Bark Extract Protects Against Oxidative Stress Induced By Recurrent Hypoglycemia In Rats.

“…These results suggested that improved state of oxidative stress as a result of the frequent lack of sugar through insulin injections was achieved by PBE treatment. The results obtained in the present study were consistent with that of [12] [14] [38] [40] on children for of GSH and TAC also with [15] for GSH, CAT and SOD, GST. Also coincided current findings regarding moral increase in the TP content in the animals treated group PBE and insulin only with the study conducted by [39], although the increase in the content of GSH in addition to increasing the activity of GST, CAT and SOD, which led to a rise in the TAC by treatment PBE due to the ability of cells to stimulate the production of components for most of the antioxidants in addition to the doubling of the cell's production of the SOD, CAT and the GSH, which represent the most powerful weapon to disable free radicals [41].…”

“…Improved liver functions can be interpreted according to the results of this study because of the improvement in oxidative stress of the liver. These results are consistent with the findings of [38] and [40] who recommended that, the use of PBE improved liver glycogen significantly, but in case of recurrent hypoglycemia the improvement was insignificant.…”

Therapeutic potential ofMoringa oleiferaextracts against acetaminophen-induced hepatotoxicity in rats

“…Acute injury to hepatocytes alters their transport function and membrane permeability, leading to leakage of marker enzymes from the cells (Yang et al, 2008). The intracellular mechanisms of injury due to APAP in hepatocytes are the formation of reactive metabolites, depletion of glutathione and alkylation of proteins, especially the mitochondrial proteins (Nelson & Bruschi, 2003).…”

Nrf2 pathway activation contributes to anti-fibrosis effects of ginsenoside Rg1 in a rat model of alcohol- and CCl4-induced hepatic fibrosis

“…CCl 4 is a widely used hepatoxin for animal models of liver fibrosis. It can be activated to trichloromethyl radical (·CCl 3 ) and trichloromethyl peroxyradical (·OOCCl 3 ) by CYP450 in the liver and stimulates Kupffer cells to produce ROS, which damage the liver [7,8] . In addition to the induction of oxidative stress, alcohol may upregulate the activity of P450 2E1 (CYP2E1) which catalyzes the conversion of CCl 4 into ·CCl 3 [9,10] .…”