Rivastigmine ameliorates indomethacin experimentally induced gastric mucosal injury via activating α7nAChR with inhibiting oxidative stress and apoptosis.

The current study aimed to investigate the potential ameliorative role of Rivastigmine (RIVA), the anti-Alzheimer drug, against the gastric mucosal injury caused by indomethacin (IND). The rats were divided into four groups: group I was given a vehicle as a control, group II was given RIVA (0.3 mg/kg) once daily intraperitoneal (ip) for 2 weeks, group III was given a single IP dose of 30 mg/kg IND, and group IV was given RIVA ip 2 weeks before the administration of IND. The gastric mucosal injury was detected by the estimation of ulcer index, gastric acidity, pepsin, and mucin concentrations. Malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), total nitrite/nitrate (NOx), and the expression of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), nuclear factor kappa B (NF-κB), Hemoxygenase 1 (HO-1), and caspase-3 were all measured in gastric tissue. In addition, histological assessment and proliferating cell nuclear antigen (PCNA) immuno-expression were studied. Gastric mucosal injury induced by IND was indicated by both biochemical and histopathological assessments. RIVA Pretreatment reduced ulcer index, MDA, TNF-α, IL-6, NF-κB, and caspase-3 and increased SOD, GSH, NOx, and HO-1. RIVA improved the suppressed nuclear immunoreaction for PCNA observed with IND. The current findings provide novel evidence that RIVA possesses a prophylactic action against IND-induced gastric mucosal damage in rats. Despite being a cholinergic drug that is associated with increased pepsin and stomach acidity, RIVA protected against IND-induced gastric mucosal injury via activating α7nAChR and inhibiting oxidative stress and apoptosis.

Hydrogen sulfide renal protective effects: possible link between hydrogen sulfide and endogenous carbon monoxide in a rat model of renal injury.

Hydrogen sulfide (H2S), along with nitric oxide (NO) and carbon monoxide (CO), proved to have renoprotective effects in various renal diseases. Therefore, this study investigated the renoprotective effect of H2S, in a renal injury model, and its crosstalk with other gasotransmitters such as CO. Thirty-two adult rats were divided into four groups: control, gentamicin (GEN)-treated, GEN + sodium hydrosulfide (NaHS), and GEN + NaHS + zinc protoporphyrin (ZnPP) groups. GEN was used to induce renal injury, NaHS is a water-soluble H2S, and ZnPP is a selective heme oxygenase-1 (HO-1) inhibitor used to inhibit CO synthesis in vivo. NaHS improved kidney functions in the GEN group as evidenced by significantly lower levels of renal injury markers: serum urea, creatinine, uric acid, urinary albumin excretion, and urinary albumin/creatinine. Moreover, NaHS administration to the GEN-treated group significantly lowered renal levels of NO and tumor necrosis factor-α with an increase in total antioxidant, HO-1, and interleukin-10 levels. Furthermore, NaHS administration downregulated the GEN-induced overexpression of the renal inducible nitric oxide synthase (iNOS) and upregulated the suppression of endothelial nitric oxide synthase (eNOS) with improvement in the histological examination and periodic acid Schiff (PAS) staining. However, this improvement in kidney function produced by NaHS was reduced by combination with ZnPP but still improved as compared with the GEN-treated group. The renoprotective effects of H2S can be through its effects on renal tissue antioxidants, pro-inflammatory and anti-inflammatory cytokines, and expression of eNOS and iNOS which can be partially dependent on CO pathway via induction of HO-1 enzyme.

Possible protective effect of platelet-rich plasma on a model of cisplatin-induced nephrotoxicity in rats: A light and transmission electron microscopic study.

BACKGROUND: Cisplatin (Cis), is a potent chemotherapeutic drug. However, Cis nephrotoxicity is high, thus limiting its use. Platelet-rich plasma (PRP) is an autologous product, easy to get from blood centrifugation. The aim of this study is to investigate the effects of PRP in reversing Cis-induced nephrotoxicity. MATERIALS AND METHODS: Thirty-two adult albino rats were distributed into Group I, the control group; Group II, in which the rats received Cis (5 mg·kg-1 ·day -1 , intraperitoneal); Group III and Group IV, in which the rats received Cis, followed by normal saline and PRP distribution, respectively (1 ml) over the renal surface 24 hr later. All rats were killed on the eighth day of the experiment. Histopathological changes were examined. RESULTS: Glomerular atrophy, tubular degeneration, interrupted PAS reaction, highly expressed caspase-3, and ultra-structural changes were observed after Cis injection, which improved with PRP administration. CONCLUSION: PRP reduced acute kidney injury through the epithelial GFs.

Morphometry of suprascapular notch in Egyptian dry scapulae and its correlation with measurements of suprascapular nerve safe zone for clinical consideration

The suprascapular notch is bridged by a superior transverse scapular ligament (STSL) and serves as a passage for the suprascapular nerve. The purpose of this study was to group suprascapular notches (SSN) and provide data on the association of the safe zone distances of the suprascapular nerve. Sixty-five Egyptian dried scapulae were classified into five groups; measurement of dimensions of SSN and measurement of safe zone for the suprascapular nerve were taken. The collected data were analyzed and the correlated parameters in the prevalent types of notches were done.Scapulae were classified into five groups of which the most prevalent groups were Type III (47.63%) followed by Type I (40%). The mean measurements of 'safe zone' distances vary according to the type of notch and correlate with notch dimensions. The present work displayed the anatomical variants of SSN and analyzed the measurement of safe zone distances to help the clinicians to manage different pathological conditions of the shoulder, in order to avoid iatrogenic injury

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Evidence of the protective effect of l-arginine and vitamin D against monosodium glutamate-induced liver and kidney dysfunction in rats.

Monosodium glutamate (MSG) is frequently consumed as a flavor enhancer or food additive. Possible MSG-induced injurious effects on some organs have been stated in experimental animal models. Thus, in this study we tried to clarify effect and possible mechanism of action of MSG on liver and kidney, and if this results affected by the addition of l-Arginine or vitamin D to it. Animals divided into; Control, MSG treated, MSG + vitamin D treated, MSG + L-arginine treated group. Serum separated to determine liver and kidney function parameters. Kidneys and livers dissected out for histological examination and for assay of oxidative stress markers. RESULTS: MSG increased body weight and produced liver and kidney dysfunctions. The MSG-induced oxidative liver and kidney damage was proved. Vitamin D and l- Arginine have been shown to protect and restore the liver and the kidney capabilities in MSG models injury via inhibiting oxidative damage, vitamin D or l- Arginine suppresses the increased food intake and body weight gain induced by MSG. CONCLUSIONS: due to injurious effect of MSG, it should be avoided especially in liver or kidney disorders, foods containing excess MSG can be fortified with vitamin D or l- Arginine to overcome its adverse effects.

Antioxidant, anti-inflammatory, and anti-apoptotic effects of zinc supplementation in testes of rats with experimentally induced diabetes.

One of the major obstacles that males with diabetes may confront is subfertility or infertility. Thus, the present study investigated the effect of co-administration of metformin and zinc (Zn) on the testes of streptozotocin-induced diabetic rats. Male albino rats were randomly divided into 4 groups: control group; untreated diabetic group; diabetic + metformin group, in which diabetic rats were treated orally with metformin (250 mg/kg) once daily for 4 weeks; and diabetic + metformin + Zn group, in which diabetic rats were treated orally with metformin in combination with Zn (10 mg/kg) once daily for 4 weeks. Concomitant administration of metformin and Zn produced a significant decrease in serum levels of glucose and insulin and testicular levels of malondialdehyde and tumor necrosis factor α. Additionally, there was a significant increase in serum levels of Zn, testosterone, and follicle-stimulating hormone, as well as testicular total antioxidant capacity and anti-apoptotic protein Bcl-2, when compared with both the diabetic and metformin-treated diabetic groups. Moreover, co-administration of Zn and metformin significantly improved testicular histopathology, with a significant reduction in percent area of collagen fibers and nuclear factor kappa B (p65) immunoreactivity and a significant increase in seminiferous tubule diameter and connexin 43 immunoreactivity as compared with the diabetic and metformin-treated diabetic groups. In conclusion, the combination of Zn and metformin was an efficacious and safe alternative treatment, as it had superior antihyperglycemic efficacy and provided additional benefits over metformin alone in rats with type 2 diabetes.