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In this study, kaempferol (KFL) shows hepatoprotective activity against zearalenone (ZEA)-induced oxidative stress and its underlying mechanisms in in vitro and in vivo models were investigated. Oxidative stress plays a critical role in the pathophysiology of various hepatic ailments and is normally regulated by reactive oxygen species (ROS). ZEA is a mycotoxin known to exert toxicity via inflammation and ROS accumulation. This study aims to explore the protective role of KFL against ZEA-triggered hepatic injury via the PI3K/Akt-regulated Nrf2 pathway. KFL augmented the phosphorylation of PI3K and Akt, which may stimulate antioxidative and antiapoptotic signaling in hepatic cells. KFL upregulated Nrf2 phosphorylation and the expression of antioxidant genes HO-1 and NQO-1 in a dose-dependent manner under ZEA-induced oxidative stress. Nrf2 knockdown via small-interfering RNA (siRNA) inhibited the KFL-mediated defence against ZEA-induced hepatotoxicity. In vivo studies showed that KFL decreased inflammation and lipid peroxidation and increased H2O2 scavenging and biochemical marker enzyme expression. KFL was able to normalize the expression of liver antioxidant enzymes SOD, CAT and GSH and showed a protective effect against ZEA-induced pathophysiology in the livers of mice. These outcomes demonstrate that KFL possesses notable hepatoprotective roles against ZEA-induced damage in vivo and in vitro. These protective properties of KFL may occur through the stimulation of Nrf2/HO-1 cascades and PI3K/Akt signaling.

Background: Lepidium sativum (LS) is a very potent and often used as anti-cancer is largely limited due to the dose-related toxic effects. The present study investigated the protective role of LS that can reduce the liver injury induced by LPS.Methods: Forty white male mice were randomly divided into five groups: the vehicle control group, LPS group, LPS plus LS group, LS pretreated plus LPS group and LS + LPS + LS group. Mice were sacrificed at 2, 4, 8, 16, 24 and 48h. Blood and liver samples were collected for the experimental investigations. Biochemical analysis, histopathological studies and molecular investigation carried out for different groups used. Result: Biochemical analysis for serum AST, ALT, LDL and HDL levels were determined to evaluate liver status. Oxidative stress of liver examined through determination of oxidative enzymes. Furthermore, proinflammatory (IL-6 and TNF-α) and anti-inflammatory (IL-4 and IL-10) cytokines were investigated. Histopathological liver sections were examined to show the alterations due to LPS injection. Biochemical analysis showed a significant modulatory effect of LS on the LPS challenged mice. Histopathological studies showed that LPS caused liver alterations, such as necrosis, infiltrations of neutrophils, sinusoid congestion and hepatocellular degeneration in the liver. These histopathological modulations were significant by LS pretreatment. These findings indicate that LS has a significant hepatoprotective effect on LPS-induced liver injury in mice model.

Background: Vitamin A has potentially harmful effects on the development of chick embryos even at very low dose concentration. Vitamin A different doses cause embryotoxic and teratogenic effects on the developing of the chick embryo. Hence, due to teratogenicity of this vitamin it can be used with utmost caution during pregnancy. Methods: Fertile chicken eggs (obtained from local hatchery) were injected with three doses of Vitamin A (15 IU/ml, 30 IU/ml, 75 IU/ml) into the center of the egg yolk. Morphometric parameters as mortality rate, body weight (g), crown rump length (mm) of embryo and Frequency % of different anomalies gross malformations were measured. Whole chicken samples were taken by 4th, 8th and 18th incubation day. Daam, Hox and Tbx genes expression profile were analyzed. Result: Dose-dependent defects and embryo lethality in the chick embryos developed when exposed to higher concentrations. Our study record for the first time the duplication in the heart, brain and eye. Also showed duplication of the neck forming S-shaped showed in some malformed chick embryos. The three investigated genes showed different fluctuations confirming the malformations detected.

Four thousand two hundred hatching eggs were obtained from Bandarah chicken to evaluate the effect of chemical and natural egg disinfectants and fumigation on egg weight loss, embryonic mortality, hatchability, hatch time, chick weight and chick weight loss. Three incubation trials were done; each one contained 1400 hatched eggs and divided into fourteen treatments (100 eggs per each). First treatment (T1) was used as control without any treatment, eggs of second treatment (T2) were dipped in water and third treatment in alcohol, whereas T4, T5, T6, T7 treated egg groups were dipped in chemical disinfectant (sodium chloride, betadine, hydrogen peroxide, virkon S). Egg of T9, T10, T11, T12, T13 and T14 groups were dipped in natural disinfectants (oregano, cumin 02 and 04 % and oregano+ cumin01 and 02), respectively. The thickest eggshell (031mm) was recorded for betadine group in infertile eggs compared with those for formaldehyde fumigation and oregano+cumin 01% oregano+cumin 01% group (035mm) compared with all other treatment groups. Formaldehyde fumigation recorded the worst and highest significant percentage of embryonic mortality (1795%). Highest significant percentages for hatchability of fertile egg were recorded in egg groups with oregano 02 and 04% (9687 and 9576%), cumin 02 and 04 % (9551and 9715%) and oregano+cumin01 and 02% (9619 and 9615%), respectively.