the current study Included, evaluation the impact of Nitrofurantoin drug on liver in albino mice, 128 male albino mice have been used . Animals treared with (150,200 Mg/Kg) for 8 weeks . NFI caused histological changes in liver represented by , swelling of hepatocytes, disappearance of radial arrangement , vaculation of liver cells , increasing of kupffer cells and appearance of giant cells. NFT caused Congestion of blood vessels and infiltration of inflammatory cells in liver in all used concentrations.

The heavy metal cadmium is extremely harmful to both humans and animals. Zinc supplementation protects the biological system and reduces cadmium-induced toxicity. This study aimed to determine whether zinc chloride (ZnCl2) could protect male mice with the damaged liver induced by cadmium chloride (CdCl2). The protective role of zinc chloride and expression of the metallothionein (MT), Ki-67, and Bcl-2 apoptotic proteins in hepatocytes were studied after subchronic exposure of mice to cadmium chloride for 21 days. Thirty male mice were randomly categorized into 6 groups (5 mice/group) as follows: a control group that did not receive any treatment, a group given ZnCl2 at 10 mg/kg alone, and two groups received ZnCl2 (10 mg/kg) i

Asthma is a chronic inflammatory disease of airways mediated by T-helper 2 (Th2) cells involving complex signaling pathways. Although resveratrol has previously been shown to attenuate allergic asthma, the role of miRNA in this process has not been studied. We investigated the effect of resveratrol on ovalbumin-induced experimental allergic asthma in mice. To that end, BALB/c mice were immunized with ovalbumin (OVA) intraperitoneally followed by oral gavage of vehicle (OVA-veh) or resveratrol (100 mg/kg body) (OVA-res). On day 7, the experimental groups received intranasal challenge of OVA followed by 7 days of additional oral gavage of vehicle or resveratrol. At day 15, all mice were euthanized and bronchioalveolar fluid (BALF), se

The current study designed to determine the effect of Glucosamine sulfate on the liver tissue of Albino mice .the study included (40)mice divided in to 4 groups(control group had distilled water orally ).The other groups treated with(1000,2000,3000)ml/k .respectively for 8 week .the liver have been taken from dissected animal for microscopic preparation to study the histological changes .Frequently histopathologicale changes appeared in the liver tissue of the exposure groups during (4-8)week .This changes depends on (Dose and Time ). The effects were Congestion ,Infiltration ,Swelling ,Vaculation ,Hyalinization , Amyloid and Necrosis.

     The metformin drug  is anti-hyperglycemia  and known to cross the placenta  which leads to the fetus during pregnancy .The aim of this study is to  define the drug  effects in the fetus growth . The doses  used , therapeutic dose ( 0.18 & 0.53 ) mg\25g body weight  and over dose ( 1.8 & 2.85) mg\ 25g body weight , administrated orally  at the beginning organogenesis stage at ( 6 -18 ) day of pregnancy in the morning . A total ( 50 ) animal  were divided into five groups .The first group control not treated , 2nd group  treated with (0.18) mg , 3rd group  with  ( 0.53 ) mg , 4th group with ( 1.8 ) mg and 5th group

In the present study, the effects of brake pad particles of lung and liver histological sections were evaluated for (60) adult male mice. The animals were divided into three groups ( A,B,C) according to the periods of exposure (4, 8, and 12) weeks respectively exposed to brake pad particles in addition to the control groups (F) exposed to fresh air only. A special inhalation chamber designed locally has been used to expose the animals. The exposure to brake pad particles was (2.228) µg/m³ for 30 min/day, 5 days/week for (4,8and12) weeks respectively.

The examination in group (A) of the histological sections of the lung showed the thickness of interalveolar septa.  Also, a congestion of alveolar capillary was marked indicat

Nonalcoholic fatty liver disease (NAFLD) is a common liver disease that ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). So far, the underlying mechanism remains poorly understood. Here, we show that hepatic carboxylesterase 2 (CES2) is markedly reduced in NASH patients, diabetic db/db mice, and high‐fat diet (HFD)‐fed mice. Restoration of hepatic CES2 expression in db/db or HFD‐fed mice markedly ameliorates liver steatosis and insulin resistance. In contrast, knockdown of hepatic CES2 causes liver steatosis and damage in chow‐ or Western diet‐fe