Testicular dysfunction is a common adverse effect of cisplatin (CIS) administration as a chemotherapeutic drug. The current study has outlined the role of micro-RNAs (miR-155 and 34c) in CIS-induced testicular dysfunction and evaluated the protective effect of N-acetyl cysteine (NAC) and/or l-arginine (LA). Seven groups of Albino rats were used for this study. The control (C) group received physiological saline; the CIS group was injected CIS (7 mg/kg IP, once) on day 21 of the experiment; the NAC group was administered NAC (150 mg/kg intragastric, for 28 days); and the LA group was injected LA (50 mg/kg IP, for 28 days). NAC+CIS, LA+CIS, and NAC+LA+CIS groups received the above regime. CIS significantly reduced serum testosterone, LH, and FSH concentrations with decline of testicular enzyme activities. CIS caused significant elevation in testicular oxidative-stress biomarkers, inflammation-associated cytokines, and apoptosis markers, along with overexpression of miR-155 and low miR-34c expression. Additionally, marked testicular degenerative changes were observed in the examined histological section; a significant decrease in the expression of PCNA with significant increase in expressions of F4/80 and BAX was confirmed. The administration of NAC or LA upregulated testicular functions and improved histopathological and immunohistochemical changes as well as miRNA expression compared with the CIS-administered group. Rats receiving both NAC and LA showed a more significant ameliorative effect compared with groups receiving NAC or LA alone. In conclusion, NAC or LA showed an ameliorative effect against CIS-induced testicular toxicity and dysfunction through the regulation of antioxidant, anti-inflammatory, and antiapoptotic markers and via modulating miR-155 and miR-34c expression.

Background: Nandrolone-decanoate (ND); is an anabolic steroid. Its toxic effects on the heart as arrhythmias, acute myocardial infarction, and sudden death have been recorded. Moringa oleifera extract (MOE); is a herbal extract used to treat various diseases due to its antioxidant effect. Aim; This study was designed to evaluate the efficacy of MOE as a protective agent against cardiotoxicity induced by ND. Material and methods ; Thirty-two adult male albino rats were allocated into four groups. Control group; MOE treated group; rats were given MOE by oral gavage (400 mg/kg/day) for four weeks. ND group; rats were injected ND S.C; at a dose of 20 mg/kg/week for four weeks. ND+MOE-treated group; rats simultaneously administrated ND; (20mg/kg/week S.C.) with MOE (400 mg/kg/day by oral gavage) for four weeks. Serum levels of cardiac enzymes were estimated. Also; MDA, GSH, SOD, IL-6, TNF- α, and IL-10 levels in cardiac tissue were estimated. Cardiac samples were processed to light, an immune-histochemical study using anti-P53 and anti-CX43 antibodies as well as electron microscopic examination. Morphometric; and statistical studies were done . Results ; In the ND group, serum levels of cardiac biomarkers and cardiac tissue levels of MDA, TNF-α, and IL-6 were significantly increased with significant diminution in the activity of catalase, SOD, diminished GSH, and IL-10 in the cardiac tissues. Light; microscopic examination showed wide endomysium, inflammatory cell infiltration, and lacerated and wavy cardiac muscle fibres were observed. There was a marked deposition of collagen fibres at areas of interrupted muscle fibres. Positive; P53 immuno-expression in the nuclei and decreased expression of CX43 were observed. Ultra-structurally; interrupted myofibrils, dilated sarcoplasmic reticulum, and a disorganized intercalated disc was observed. In (ND+MOE) group; showed marked amelioration in the cardiac architecture and ultrastructure, down-regulation of P53, and CX43 immuno-expressions, and a significant reduction in serum level of cardiac biomarkers, and cardiac tissue levels of MDA, TNF-α and IL-6 with a significant increase in activity of catalase, SOD, diminished GSH and IL-10 in the cardiac tissues. Conclusion ; MOE could alleviate the cardio-toxic effects induced by ND in rats through anti-inflammatory, anti-oxidant; and anti-apoptotic effects.

Introduction: Ionizing radiation (IR) is effectively used in the treatment of oral malignancies; however, it might also significantly harm the surrounding tissues. Whey protein isolate (WP) is a protein derived from milk that exhibits a wide range of bioactivities. Therefore, the present research aimed to delineate the mitigating impact of WP against gamma irradiation-induced lingual damage.Methods: Rats were randomized into 5 groups: Control (saline, orally, 14 days), WP (WP; 0.5 g/kg b. w., orally, 14 days), IR (saline, orally, 14 days, exposed to 6 and 3 Gy on days 4 and 6, respectively), WP+IR (WP was given orally for 14 days before and after IR exposure; exposed to 6 and 3 Gy on days 4 and 6, respectively), and IR+WP (WP, orally, started 24 h after 1st IR exposure till the end of the experiment) groups. Samples were collected at two-time intervals (on the 7th and 14th days).Results and Discussion: Oxidative stress was stimulated upon IR exposure in tongue, indicated by boosted malondialdehyde (MDA) level, along with a decrease in the total antioxidant capacity (TAC) level, superoxide dismutase (SOD), and catalase (CAT) activities. Additionally, IR exposure depicted an increase of serum IgE, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-6, along with overexpression mRNA levels of nuclear factor kappa-B transcription factor/p65 (NF-κB/p65), and down-regulation of nuclear factor erythroid 2–related factor 2 (NRF2) and heme oxygenase (HO-1) mRNA levels in tongue tissue. Moreover, IR triggered alterations in lingual histological architecture. The antioxidant and anti-inflammatory properties of WP mitigated oxidative damage, inflammation, and desquamation that were brought on following IR exposure. The protective administration of WP markedly decreases IR-induced lingual harm compared to the mitigation protocol. Our findings recommend WP supplements to the diets of cancer patients undergoing IR that might aid radioprotective effects.

Lead toxicity is a common occupational and environmental health hazard that exerts many toxic effects on animals and humans, including immunotoxicity. Curcumin (CUR) and cinnamon (CIN) are common medicinal herbs with immunostimulatory and antioxidant properties. Therefore, this study investigated the protective effect of curcumin and cinnamon against lead acetate (LA)-induced splenotoxicity in rats via hemato-biochemical, immunological, oxidative stress marker, CYP-2E1 expression, histological, and immunohistological evaluations. Four groups of seven rats each were used: the control group received corn oil as a vehicle; the lead acetate group received (100 mg/kg), the CUR + LA group received curcumin (400 mg/kg) plus lead acetate, and the CIN + LA group received cinnamon (200 mg/kg) plus lead acetate orally for 1 month. LA exposure induced macrocytic hypochromic anemia, leukocytosis, neutrophilia, monocytosis, and lymphopenia. Additionally, significant elevations in serum iron, ferritin levels, and transferrin saturation percentage with significant decline of total and unsaturated iron binding capacities (TIBC and UIBC), transferrin, and immunoglobulin G and M levels were recorded. In addition, lead acetate significantly upregulated splenic CYP-2E1 expression, that was evident by significant depletion of reduced glutathione (GSH) activity and elevation of malondihyde (MDA), nitric oxide (NO), and protein carbonyl (PC) concentrations in the spleen. Histologically, hyperplasia of lymphoid follicles, hemosiderin deposition, and disturbance of CD3 and CD68 immuno-expressions were evident in the spleen from the lead acetate group. However, curcumin and cinnamon administration restored the hemato-biochemical, immunological, and oxidative stress parameters as well as histological and immunohistological pictures toward normalcy. In conclusion, curcumin and cinnamon can partially ameliorate LA-induced oxidative damage in the spleen, possibly through their antioxidant, immunomodulatory, and gene-regulating activities.

: Background: Osteoporosis (OP) is a disease characterized by decreased bone mass and is widely recognized as a major health problem. Flutamide is an androgen receptor blocker used in treatment of cancer prostate. Its prolonged use is usually associated with OP which is now treated by bisphosphonates. Aim : this work was designed to explore the potential benefit of forskolin (a cAMP/protein kinase A pathway stimulant) alone and in combination with alendronate on flutamide -induced osteoporosis in rats. Subjects and methods: Forskolin 6 mg/kg/day orally was taken either singly or in combination with Alendronate 0.1mg/kg /day orally in rat model with osteoporosis which was induced by flutamide 15 mg/kg/day orally for 4 weeks (in a three-months case-controlled study, at clinical pharmacology