Background: Renal replacement therapy, either by transplantation or dialysis, is not accessible in many parts of the world because of lack of financial and clinical resources. This study was performed to investigate the nephroprotective efficiency of gum arabic (GA) and lemongrass (LG) on adenine-induced chronic kidney disease. Materials and methods: Four animal groups (each of 10 rats) received normal saline, intraperitoneal injection of adenine (300 mg/kg) twice a week, and adenine plus oral GA (5.4 g/kg) or oral LG (360 mg/kg) daily for 4 weeks. Results: Compared to control group, adenine-injected rats had significantly higher levels of serum urea, creatinine, and uric acid. Moreover, biochemical analysis of kidney homogenate showed that adenine injection was associated with significantly higher levels of malondialdehyde and lower levels of reduced glutathione and antioxidant enzyme activities in comparison with normal control. Additionally, the adenine group exhibited a significant upregulation in tumor necrosis factor-α and downregulation in interleukin-10 gene expression. Histopathological and immunohistochemical examinations of renal tissue from the adenine group showed degeneration to renal glomeruli and renal tubules with increased DNA double-strand breaks. On the other hand, treatment with GA or LG ameliorated all the previous parameters to a large extent. Conclusion: From this study, we concluded that oral administration of GA or LG could conceivably alleviate adverse effects of CKD which might be ascribed to their antioxidant and free radical-scavenging properties.

Cadmium (Cd) is wide-spread toxic metal that pollutes most of the vegetables, which eaten by numerous populations all over the world. The aim of the current work is to evaluate the protective and prophylactic effects of the antioxidant materials in the grape seed extract (GSE) on the hepatic intoxication induced by cadmium chloride toxic material in male Wistar rats. Male adult Wistar rats were divided into four groups. Control group fed on balanced diet and given drinking water. Group two (control positive) given CdCl2 in the dose of 0.44 mg/kg body weight (BW) by stomach tube daily. Group three given grape seed extract GSE in the dose of (100 mg/kg BW) daily by stomach tube. Finally, the fourth group gave mixture of (GSE and CdCl2) by stomach tube in the recommended dose. Blood and liver tissues were collected for further biochemical and histopathological studies. CdCl2 significantly increased the serum levels of malondialdehyde, ALT and AST. Cadmium administration decreased levels of antioxidants (Catalase, GSH-R and GSH-Px). The liver of the control positive groups which given CdCl2 showed degenerative changes in the form of vacuolar and hydropic degeneration. Congestion was evident in the central vein and proliferation of the kupffer cells. These hepatic biochemical and degenerative changes were ameliorated by the co addition of GSE.

The biochemical effect of Chitosan on hepatic lipid metabolism in experimental induced Nonalcoholic fatty liver disease (NAFLD) in rats was investigated. Thirty male albino rats were divided into three groups (10 rats each). Group I (control group): rats was fed on normal diet. Group II (NAFLD Group): rats fed on normal diet enriched with 1% cholesterol and 2% coconut oil. Group III (Chitosan treated group): rats fed on normal diet enriched with 1% cholesterol and 2% coconut oil and supplemented with Chitosan 5%. Blood samples were collected after 2, 4 and 6 weeks from the onset of chitosan treatment. All serum were directly used for determination of total cholesterol (TC), triacylglycerol (TAG), low density lipoprotein cholesterol(LDL-C), very low density lipoprotein cholesterol (VLDL-C), high density lipoprotein cholesterol (HDL-C), total lipids,(TL) Phospholipids, Non esterified fatty acids (NEFA) , apo-lipoprotein-B (Apo-B), tumor necrosis factor alpha (TNF-α) , interleukin-6(IL-6). the obtained results showed a significant increased in serum TC, TAG, LDL-C, VLDL-C,TL, phospholipids, NEFA and Apo-B concentrations with a marked decrease in HDL-C level .Also, serum TNF-α ,IL-6 was significantly increase in NAFLD group was observed. The results mentioned that treatment with Chitosan to NAFLD induced rats showed a significant change and ameliorate in all parameters nearly normal level that indicated the Hypolypidemic and anti-inflammatory effect of Chitosan in NAFLD induced rats.

The main objective of this study is to investigate the alterations of resveratrol on oxidative stress in experimental induced nonalcoholic fatty liver disease (NAFLD) in rats. Thirty male albino rats were divided into three groups (10 rats each). The first group fed a normal diet and represents the control group. The second group (NAFLD) fed normal diet enriched with1% cholesterol and 2% coconut oil and act as positive control. The third group fed on normal diet enriched with1% cholesterol and 2% coconut oil and Resveratrol at a rat dose3mg/kg body weight / daily /6weeks intra peritoneal (i.p). Samples collected after 2, 4 and 6 weeks after treatment. serum was used for estimation of serum nitric oxid (NO), L-Malondialdehyde (L-MDA) and Immunoglobulins as serum Immunoglobulin A (IgA) Immunoglobulin G (IgG) and liver function tests as serum Aspartate aminotransferase (AST) ,serum Alanine amino transferase (ALT), serum Gamma glutamyl transferase (GGT). Hepatic tissues for Enzymatic Antioxidants as Liver Catalase (Liver CAT),Liver superoxide dismutase(Liver SOD) ,Non Enzymatic Antioxidants as Liver Reduced Glutathione (Liver GSH). Results revealed a significantly decrease in serum NO ,Liver CAT, Liver SOD, Liver GSH More ever serum L-MDA, serum AST ,ALT, GGT were significantly increase concentration In addition to Serum IgA, IgG were also significantly increase .The behavioral biochemical results indicated treatment with Resveratrol showed a significant changes and improves these parameters.

Publications concerning the protective effect of pectin against lead induced toxicity in rats are not available. In order to study such effect, 40 male rats were divided into 3 groups. The first group was contained 10 rats that kept as control group. The second group was contained 10 rats that received pectin at dose of 100 mg/kg BW during experimental period (8 weeks). The third group was contained 20 rats that received 400mg/kg BW of lead acetate daily for 4 weeks then divided into two subgroups (3A and 3B). Subgroup 3A contained 10 rats that still receive lead acetate in the same dosage whereas, subgroup B co-treated with lead acetate and pectin daily for another 4 weeks. Blood samples were collected after 2, 4 and 8 weeks from the start of the experiment. Liver, kidney and bone marrows were collected only at the end of the experiment. Lead acetate induced anemia only after 4 weeks of administration as reflected on decreased values of Hb, PCV, MCV, MCH and MCHC. These indices remained at lower levels in lead acetate treated groups until the end of the experiment. Concentrations of serum ferritin, iron, total antioxidant capacity (TAC) and reduced glutathione (GSH) and the expression of hepatic hepcidin gene were decreased significantly in lead acetate intoxicated rats compared to control. Activities of ALT and AST and concentrations of urea, creatinine, Nitric oxide (NO), TNF-α, IL-6, total iron binding capacity (TIBC) and lead were increased significantly in lead acetate intoxicated group compared to control. Hepatic degeneration and hemorrhage, renal lytic necrosis and apoptosis of myeloid cells were most prominent changes in lead intoxicated rats. Lead acetated related changes were improved by co-treatment with pectin however; normal control values have not been achieved. Conclusively, pectin is recommended to protect against lead acetate toxicity in rats. Key words: lead acetate; toxicity; pectin; hepcidin; oxidative stress biomarkers; histopathology