F errous sulfate is the most commonly used drug for treatment of iron deficiency anemia, but it is badly absorbed and causes many unfavorable side effects. Nanotechnology is a way to decrease the side effects of drugs and to increase the drug bioavailability. So, this study is designed to investigate the effect of iron oxide nanoparticles in comparison to ferrous sulphate in the treatment of iron deficiency anemia in rats. Forty male albino rats were divided into two main groups: Control group (10 rats) and anemic group (30 rats) that received standard iron free basal diet for six weeks. Then the anemic group was subdivided into three groups (10 rats) in each group: anemic control group, ferrous sulfate group (received ferrous sulfate 0.4 mg/ kg b.w/ 10 days) and iron oxide nanoparticles group (received iron oxide nanoparticles 0.4 mg/ kg b.w/ 10 days) in the drinking water. Iron oxide nanoparticlescaused a significant increase in the level of red blood cells (8.80±0.05 10 6 /µL), hemoglobin (18.46±0.33 g/dL), hematocrit (46.66±0.23 %), mean corpuscular volume (MCV) (53.02±0.3 FL), mean corpuscular hemoglobin concentration (MCHC) (39.56±0.6 %), ferritin (447.6±9.02 µg/L), transferrin saturation (138.0±1.5), total iron binding capacity (TIBC) (145.00±1.15 mg/dL) and serum iron (276.33±2.07 mg/dL). Moreover, it decreased serum malondialdehyde (MDA) (31.85±0.34 nmol/g) and C-reactive protein (CRP) (312.66±1.7 mg/L) when compared to ferrous sulfate group and anemia control groups. These results revealed that iron oxide nanoparticles proved as an effective drug for the treatment of iron deficiency anemia in rats.

It is concluded that coconut oil is very effective against deleterious hyperlipidemic, hyperglycemic and nephro-toxic effects of alloxan.

Objective: The main objective of this study is to investigate the antioxidant and nephroprotective efficacy of moringa oleifera seed extract (MOSE) against cisplatin which induced acute renal injury. Methods: Forty male Wister rats were equally segregated into 4 groups (10 rats per group): group I (0.5 ml of sterile saline orally), group II (200 mg MOSE/kg b. wt orally for 10 consecutive days), group III (7.5 mg cisplatin/kg b. wt/intraperitonially as a single dose on the 5th day of the experiment) and group IV (200 mg moringa oleifera seed extract (MOSE)/kg orally for 10 d followed by 7.5 mg cisplatin/kg body weight/intraperitonially once as a single dose on the 5th day of the experiment. Serum biochemical analysis of renal biomarkers (urea, uric acid, and creatinine), oxidative stress markers (malondialdehyde [MDA]), a crucial antioxidant enzyme (catalase) and the expression of renal activity interleukin (IL)-6, (IL)-10 and Tumer necrotic factor (TNF-α) mRNA were determined. Histopathological examination of renal tissue was done. Results: Cisplatin induced renal damage, increased renal biomarkers (urea, creatinine and uric acid)(375.87±1.65, 5.238±0.25, 4.47±0.25). Tissue concentrations of malondialdehyde, IL-6 and TNF-α.(387.56±0.97, 2.188±0.20, 3.06±0.27)compared to control group(140.58±1.25,0.938±0.017, 1.24±0.17), (163.99±1.34, 1.008±0.05, 0.982±0.026) Moreover, cisplatin induced significantly down-regulation of anti-inflammatory (IL-10) and catalase (0.780±0.47, 1.62±0.06) compared to control one (1.010±0.02, 3.12±0.11),. The histopathological examination showed renal tissue damage and degeneration of tubules in the cortical portion in cisplatin group. However, interestingly concurrent adminsteration of the MOSE with cisplatin can alleviated the renal damage, oxidative stress and renal toxicity caused by cisplatin. Conclusion: These results suggest that the antioxidant and the anti-inflammatory effects of MOSE alleviate the cisplatin-induced nephrotoxicity.

Aflatoxins (AFs) are the most detrimental mycotoxin, potentially hazardous to animals and humans. AFs in food threaten the health of consumers and cause liver cancer. Therefore, a safe, efficient, and friendly approach is attributed to the control of aflatoxicosis. Therefore, this study aimed to evaluate the impacts of Chlorella vulgaris (CLV) on hepatic aflatoxicosis, aflatoxin residues, and meat quality in quails. Quails were allocated into a control group; the CLV group received CLV (1 g/kg diet); the AF group received an AF-contaminated diet (50 ppb); and the AF + CLV group received both treatments. The results revealed that AF decreased the growth performance and caused a hepatic injury, exhibited as an increase in liver enzymes and disrupted lipid metabolism. In addition, AF induced oxidative stress, exhibited by a dramatic increase in the malondialdehyde (MDA) level and decreases in glutathione (GSH) level, superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Significant up-regulation in the inflammatory cytokine (TNF-α, IL-1β, and IL-6) mRNA expression was also documented. Moreover, aflatoxin residues were detected in the liver and meat with an elevation of fat% alongside a decrease in meat protein%. On the other hand, CLV supplementation ameliorated AF-induced oxidative stress and inflammatory condition in addition to improving the nutritional value of meat and significantly reducing AF residues. CLV mitigated AF-induced hepatic damage, decreased growth performance, and lowered meat quality via its antioxidant and nutritional constituents.

The present study was designed to investigate biochemical changes induced by doxycycline treatment of carrageenan-induced renal inflammation. For this purpose, 60 rats divided into four groups. Group (1) used as a control and administrated distilled water (1 ml/kg, i. p.) daily for 5 days. Group (2) carrageenan group: rats administrated 2% λ-Carrageenan (25 µl/ kg, i. p.) as one dose at first day of experiment. Group (3) doxycycline rats were received doxycycline (100 mg/kg, i. p./day/5 days). Group (4) carrageenan+ doxycycline rats were received doxycycline (100 mg/kg, i. p.), after an hour 2% λcarrageenan (25 µl/kg, i. p.) as one dose at first day of experiment. The experiment was continued for 5 days. Collection of samples was performed on 1 st , 3 rd , and 5 th day of experiment. Serum was used for evaluation of kidney function (urea, creatinine, Na + and K + ) and plasma proteins (total protein, albumin, and globulin), as well as inflammatory markers and cytokines (TNF-α, IL-6, CRP, and NO). Kidney tissue used for estimation of antioxidant parameters (MDA and GPx), and histopathology. The results revealed that there were significant increases in urea, creatinine, MDA, TNF-α, IL-6, CRP, and NO in carrageenan group, while GPx, Na + and K + showed significant decreases. Moreover, histological examination of group 2 showed degenerative changes in the lining epithelium of renal tubules associated with peritubular mononuclear cells infiltration compared with control group. Therefore, it could be concluded that doxycycline has anti-inflammatory role.

Salinity stress is one of the marked influencing factors on the ecophysiology of aquaculture and is considered an important reason for the retreat of the fish industry. The current study is an endeavor to elucidate the molecular mechanisms that underlie the response to salinity stress in common carp. Fish (Average weight 5 ± 2 g) were randomly distributed into two groups; the 1st is a control was exposed to tap water (0.2 ppt salinity) and the 2nd is a treated was exposed to hypersalinity (10 ppt salinity) for five days. Serum biochemical indicators including total protein, albumin, globulins, A/G ratio, blood glucose, cortisone, Na+, K+, and Cl- levels were evaluated. Besides, Tumor necrosis factor-α, interleukin-1β, corticotropin-releasing hormone, and catalase enzyme mRNA expression levels were assessed in lymphoid and immunocompetent organs (liver and spleen) and osmoregulatory organs (kidney and gills) by using Real-time qPCR. Hypersalinity adversely affected the biochemical markers; total protein, albumin, and globulins decreased significantly; however, blood glucose, serum cortisol, and sodium markedly increased in fish exposed to hypersalinity compared with the control. In addition, from the molecular point of view, all the evaluated genes were upregulated at a high expression rate in the liver compared with other studied organs after the salinity challenge. On the contrary, hypersalinity modulated the expression of immune-related genes (Tumor necrosis factor-α and interleukin-1β) in the kidney and spleen and upregulated corticotropin-releasing hormone mRNA in all studied organs except gills. In conclusion, the obtained data clarified the molecular and biochemical mechanisms of salinity stress on the liver, kidney, spleen, and gills. Furthermore, it strongly suggests the implication of neural, endocrine, and immune systems in the responsive mechanisms to the salinity stress in carp.

2013).Traditional plant medicines or herbal formulations might offer a natural key to hepatoprotective effect against xenobiotic/drug(Mukazayire, Minani et al. 2011). Flavonoids are natural polyphenols found ubiquitously in various fruits, leaves and seeds(Kumar and Pandey 2013).Rutin is a common dietary flavonoid that possesses a wide spectrum of biochemical and pharmacological actions due to their anti-oxidative and free-radical scavenging properties (Kampkötter, Nkwonkam et al. 2007).It is a well-established that N-acetyl cysteine is a cytoprotective drug with high efficacy against drug induced hepatotoxicity (Cetinkaya, Bulbuloglu et al. 2006).Therefore, we aimed in the present study to evaluate the diagnostic value of hepatocyte-derived microRNAs in detection of experimentally induced liver affection by INH in rats via evaluation of microRNAs, their genes, oxidants and anti-oxidants. Materials and Methods:-Experimental animals:Nineteen male Wister rats aging 3 weeks (130-150 gm)were obtained from the Animal House, Faculty of Veterinary Medicine Benha University, Egypt. All animals were caged and maintained on a standard diet with free access to tape water and were acclimatized for 1 week before starting the experiments. Chemicals:Isoniazid was obtained from Medical Union Pharmaceuticals Company and was given as intraperitoneal injection of 100 mg/kg body weight once daily for 21 days as previously described (varkey and Vahab 2016)Rutin was obtained from El Qahera Company andadministered to rats at a dose of 200 mg/kg body weight through oral intubation, once a day for 21 days as previously described(Abdel-Raheem 2010).N-Acetyl cysteine was obtained from SEDICO Company and was given 300mg/kg/day orally for 21 days as previously described (Hemalatha, Reddy et al. 2013). Experimental design:72 adult male Wistar rats (130-150 gm) were divided into six groups each group12 rat:Control group:received 1ml sterile saline /Kg/b.wtI/P.INHgroup: received a single doseof 100 mg INH /kgb.wt/day I/Pfor 21 days.INH + Rutingroup: wasgiven a single doseof 100 mg INH /kgb.wt/day I/P for 21 days and were treated with 200 mgrutin/kg/day b.wtorally for 21 days. INH + NAC group: was given a single dose of 100 mg INH /kg b.wt/day I/P for 21 days and was treated with 300 mg NAC /kgb.wt/day orally for 21 days.Rutingroup:was given 200 mgrutin/kgb.wt/day orally for 21 days.NAC group: was given 300 mg NAC /kg b.wt/day orally for 21 days. Assay methods: Tissue Samples:Specimens from liver was collected from all groups after sacrificing at 14 and 21 days and preserved frozen for miRNAs, genes measurements, oxidants and anti-oxidantsdetermination.Molecular investigation using real time PCR: Cyclin G1 and STAT 3 genes: RNA extraction from liver tissues Pure RNA was extracted using total RNA Purification Kitaccording to the manufacturer protocol (Laudadio, Manfroid et al. 2012K0731). cDNA synthesis: Reverse transcription kits (Thermo Scientific, Fermentas, #EP0451)This technique was done using Revert Aid H minus Reverse Transcriptase whichi...