administration of BM-MSCs during induction of ADR nephropathy provides partial protection, which could be due to improvements in the levels of of endogenous antioxidants, reduction of apoptosis, and maintenance of the integrity of the glomerular membrane.

No abstract

Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction.

Estimation the degree of induced hemisection damage of the cervical segments of the two separately diaphragmatic pillars in rat model using Electromyography (EMG). Design: Prospective controlled study. Animals: Sixteen Sprague dawely rats were divided into 2 groups Procedures: Cervical hemi lateral cord section below the cervical dorsal root number 2 was induced with micro scalpel. After 28 days post-injury, EMG record was done at the two diaphragmatic crural regions, followed by histopathological and immunohistochemical examinations. Results: There was significant decrease in mean integrated EMG activity of LT diaphragmatic muscles than RT one in the hemi sectioned group P<0.05. Moreover, there was a significant decrease (P<0.05) in the integrated traces (mv) for peak burst area of LT diaphragmatic muscles activity. On histopathological examination, affected neurons of hemi-sectioned group appeared shrunken with chromatolysis, others were completely lost and replaced by cavities. The neutrophil adjacent to the necrotic neurons lost its homogeneous appearance and appeared vacuolated or edematous with significant decrease in the number of viable motor neurons compared to the control group (P < 0.05). On other hand, the astrocytosis become more evident and the number of astrocytes was significantly increased (P < 0.05). The surrounding white matter exhibited severs degeneration and demyelination. Glial fibrillary acidic protein (GFAP) immune expression for hemi-sectioned group was significantly increased than control group (P < 0.05) Conclusion and clinical relevance: Parallel impairment of the diaphragmatic EMG occurred to the decrease in the number of viable motor neurons of the anterior horn of the cervical segment below the level of the cervical hemisection together with the disintegration of Nissl bodies and the developed astrocytosis.

The aim of this study was to investigate the possible protective role of Hydrogen sulfide (H 2 S) on chronic unpredictable stress (CUS) -induced gastric lesions in rats. Materials and methods: 40 rats were divided into 4 groups: control group, stressed rats group, stressed + Aminooxyacetic acid (AOAA) (inhibitor of H 2 S synthesis; 50mg/kg/48hour; IP), stressed + Sodium hydrosulfide (NaHS) (donor of H 2 S, 5mg/kg/48hour; IP). In all the groups exposed to CUS, a set of chronic unpredictable stressors was applied for 6 weeks in random order. At the end of experimental protocol blood samples, gastric content and gastric tissues samples were collected. Gastric tissues histopathological changes were evaluated by macroscopic and microscopic examination. Gastric content pH, serum MDA level, whole blood GSH level were estimated. Expression of Caspase-3 (apoptotic marker) and BCL-xl (anti-apoptotic marker) was assessed by immunohistochemistry. Results: In all the groups exposed to CUS, there was a significant reduction in gastric pH value and a range of gastric lesions ranging from superficial to deep ulceration as evident by macroscopic and microscopic examination. Also, there was significant elevation in MDA serum level and significant reduction in anti-oxidant GSH blood level. In all stressed rats, the expression of Caspase-3 was significantly higher whereas a significant decrease in expression of anti-apoptotic protein BCL-xl was observed. These findings were aggravated by AOAA while using NaHS improved them. Conclusion: it seems that increasing bioavailability of H 2 S could have a protective role against CUS induced gastric lesions. The results suggest that this protection could be through anti-oxidant and anti-apoptotic effects Keywords• hydrogen sulfide (H2S)• Chronic unpredictable stress (CUS)• Caspase 3Bull. of Egyp. Soc. Physiol. Sci.