Diabetic retinopathy (DR) is the most feared ocular manifestation of diabetes. DR is characterized by progressive retinal damage that may eventually result in blindness. Clinically, this blindness is caused by progressive damage to the retinal microvasculature, which leads to ischemia, retinal swelling, and neovascularization. Retinopathy is associated with both type 1 and type 2 diabetes, with DR being the leading cause of new onset blindness in United States adults. Despite this strong association with diabetes, it must be noted that the development of retinopathy lesions is multifactorial and may occur in individuals without an established history of diabetes. Metabolic syndrome is a multifactorial condition of central obesity, hypertriglyceridemia, dyslipidemia, hypertension, fasting hyperglycemia, and insulin resistance. Although several studies examined the individual components observed in the metabolic syndrome in relation to the development of DR, there is conflicting data as to the association of the metabolic syndrome with the development of retinopathy lesions in non-diabetic subjects. This review will summarize the current literature on the evidence of the metabolic syndrome on retinopathy in subjects with and without an established history of diabetes. This review will also discuss some of the mechanisms through which metabolic syndrome can contribute to the development of retinopathy.

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Available online xxx Keywords:Liver fibrosis Glycyrrhizin Omega-3 fatty acids NF-kB MDA a b s t r a c t Nuclear Factor kappa B (NF-kB) is a key transcriptional regulator that plays important roles in the pathogenesis of hepatic inflammation and fibrosis in chronic liver diseases.NF-kB activation leads to production of pro-inflammatory and fibrogenic cytokines.Glycyrrhizin (GL) is reported to suppress liver fibrosis and cirrhosis. Omega-3 fatty acids (u-3) play an anti-inflammatory role and they are reported to decrease hepatic injury in Thioacetamide (TAA) fibrotic model. We investigated the effects of GL and u-3 on liver inflammation and fibrosis in rats and clarified the effects of these natural compounds on NF-kB level. 50 male Wistar rats randomized to 5 groups: Control group and 4 groups received TAA 200 mg/kg i.p. twice weekly for 8 weeks: TAA group, GL group (received GL 25 mg/kg daily by oral tube), u-3 group (received u-3150 mg/kg daily by oral tube), (GL þ u-3) group (received similar combined doses of both natural compounds). GL and u-3 alone or in combination protected the liver from TAA hepatotoxic effects as they significantly decreased serum AST activity and serum total bilirubin level, they also significantly increased serum albumin and total protein levels. The hepatoprotective effects of GL and u-3 were confirmed by the histopathological analysis as they significantly reduced the necroinflammatory scores and the extent of fibrosis. GL and u-3 significantly decreased liver malondialdehyde level (P < 0.005), liver NF-ƙB level (P < 0.005) and its tissue expression as detected by immunohistochemistry. In conclusion, glycyrrhizin and omega-3 fatty acids alone or in combination have potent antiinflammatory, anti-oxidant and anti-fibrotic effects.Please cite this article in press as: Abo El-Magd NF, et al., Hepatoprotective effects of glycyrrhizin and omega-3 fatty acids on Nuclear Factor-kappa B pathway in thioacetamide-induced fibrosis in rats, Egyptian Journal of Basic and Applied Sciences (2015), http://dx.

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