The purpose of the current investigation is to determine how soy isoflavone (ISF) and genistein (GS) affects oxidative stress, IL1-ß and PPARγ signaling pathways in liver of obese rats and how this pathway is involved in controlling the formation of hepatic fat. The study included 60 male Sprague Dawley rats that were allocated to six groups (n = 10rats) :(I) Fatty liver was induced in rats were daily fed  (60% fat energy, high fat diet (HFD)) for 12 weeks ; (II) (Fatty liver + ISF group)  rats were daily fed with HFD and 10 mg/Kg ISF  intragastrical for 12 weeks ;(III) (Fatty liver + GS group)  rats were given HFD and 16 mg/Kg GS in 0.1%  DMSO once daily by intragastric tube for 12 weeks; (IV) (Normal control group) rats were fed with normal balanced diet for 12 weeks; (V)(Normal diet + ISF group) rats were fed with normal diet and 10 mg/Kg ISF  intragastrical for 12 weeks; (VI) (Normal diet + GS group)  rats were fed with normal diet and 16 mg/Kg GS for 12 weeks. All rats allowed water whereas rats got HFD were accompanied by 18% sucrose solution freely. Also, weight was measured weekly. At the end of the experiments lipid profile and liver function were analyzed. Moreover, the levels of MDA, SOD, CAT, and GSH, and the gene expression of IL1-ß and PPARγ genes were detected.  Our study showed that fat content was significantly lowered in the liver of ISF and GS  -fed obese rats, accompanied by a reduction in hepatocellular vacuolation when compared to the fatty liver control. In ISF and GS fatty liver treated groups SOD, CAT and GSH activities were significantly increased in comparison to the Fatty liver untreated group in addition to that MDA level decreased in ISF and GS groups.IL1-ß expression and PPARγ expressions was dowenregulated in Fatty liver  + ISF and  Fatty liver+  GS treated rats when compared with Fatty liver one,however the results in Fatty liver+  GS treated rats was significantly Improved over ISF +  Fatty liver.Genistein administration alleviated fatty liver  through the down-regulation of PPARγ and IL-1 β  and up-regulation the activity of oxidative stress marker ( SOD , CAT and GSH).

Objective-To study the antiviral activity of genistein, a soya isoflavone, on in vitro replication of bovine herpesvirus type 1 (BHV-1). Sample Population-Madin-Darby bovine kidney (MDBK) cells. Procedure-Effects of genistein on the magnitude and kinetics of inhibition of BHV-1 phosphorylation of glycoprotein E (gE) and in vitro replication of BHV-1 in MDBK cells were evaluated. Antiviral activity of genistein was compared with 2 compounds, estradiol-17β (EST) and tamoxifen (TAM), that have estrogenic and antiestrogenic activity, respectively. High-performance liquid chromatography (HPLC) was used to determine the concentration of genistein in medium from infected and uninfected MDBK cultures. Results-Genistein reduced BHV-1, but not gE-deleted BHV-1 (BHV-1gEΔ3.1), replication by 90% at 18 hours after inoculation. This inhibition was not sustained through 24 hours after inoculation. The genistein concentration in media from MDBK cells was decreased by 40% during BHV-1 infection, compared with 16% for uninfected cells, at 24 hours after inoculation. Genistein inhibited gE phosphorylation and BHV- 1 replication in a dose-dependent manner. Dosing with 25 µMgenistein at 0 and 12 hours after inoculation of BHV-1 was optimal for decreasing BHV-1 replication. Estradiol-17β EST and TAM did not affect BHV-1 replication. Conclusions and Clinical Relevance-The decrease in genistein concentration was a viral infection-dependent event. Genistein is an inhibitor of BHV-1 replication because of its ability to inhibit tyrosine kinase activity. A possible application may be for the control of BHV-1 infection in cattle by feeding soya products rich in genistein prior to or during periods of stress.