Investigation of Neuroprotective Effect of Shilajit Extract in Experimental Head Trauma Model Created in Rats.

AIM: To investigate the neuroprotective effect of shilajit extract in experimental head trauma. MATERIAL AND METHODS: Three groups of 33 Sprague Dawley Albino strain male rats were included in the study. Group 1 (n=11): trauma but not treated. Group 2 (n=11): trauma and treated with 0.5 mL / rat saline Group 3 (n=11): 150 mg / kg shilajit extract was administered intraperitoneally in the treatment of trauma. Following the head trauma, the indicated treatments were applied to the 2nd and 3rd groups at the first, twenty-four and forty-eighth hours. Brain tissues and blood samples were taken after the control animals were sacrificed at the 72nd hour in all groups after trauma. Sections prepared from cerebral cortex and ca1 region were examined with hematoxylin eosin and luxol fast blue staining. Total antioxidant capacity, total oxidant capacity and oxidative stress index were measured from blood samples taken after routine procedures. RESULTS: The number of red neurons and the severity of edema were significantly higher in both the cerebral cortex and the ca1 region in the group treated with trauma only and in the group administered saline after trauma compared to the group that received shilajit extract after trauma. The total antioxidant capacity increased significantly in blood samples taken only from the group treated with trauma and saline in post-trauma treatment compared to the group given post-traumatic shilajit extract, while shilajit extract given due to traumatic brain injury significantly decreased the total oxidant capacity and oxidative stress index values compared to the other groups. CONCLUSION: Shilajit extract has been shown to have a neuroprotective effect in the treatment of acute traumatic brain injury. Our study showed that shilajit may be a useful option in the treatment of secondary brain injury, in humans.

Effect of fulvic acid on gastric mucosa damage caused by chronic water avoidance stress.

We investigated the antioxidant and anti-ulcerogenic effects of fulvic acid (FA) on oxidative damage caused by water avoidance stress (WAS) in rat gastrointestinal mucosa. Three experimental groups were established: control (C), chronic stress (CS), and chronic stress + FA (CS + FA). After WAS, a single dose of FA was administered for 10 days to the CS + FA group. Samples of the pyloric region of the stomach were stained with hematoxylin and eosin (H & E) and periodic acid-Schiff (PAS). Immunohistochemical staining was performed for inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS). Total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) levels were measured biochemically. By light microscopy, we observed loss of gastric epithelial cells and greater polymorphonuclear cell migration into the mucosa in the CS group compared to the C group. We found intact epithelial cell structure and a thick superficial mucus layer in the CS + FA group compared to the CS group. These findings in the CS + FA group were similar to those for group C. iNOS staining was stronger in the CS group compared to the C group. TOS and OSI levels in the CS + FA group were decreased compared to the CS group, but TAS, SOD, GPx and CAT levels were increased. We found that WAS caused damage to epithelium and connective tissue of the stomach mucosa and that this damage was prevented by FA. Therefore, administration of FA appears to prevent stress induced damage to rat stomach.

The antioxidant and antiapoptotic effect of boric acid on hepatoxicity in chronic alcohol-fed rats.

The harmful use of alcohol is a worldwide problem involving all ages. This study aims to investigate chronic alcohol exposure related hepatotoxicity on the rat liver and possible hepatoprotective effects of boric acid. Rats were separated into 4 different groups: control, ethanol, ethanol+boric acid, and boric acid. We measured (i) malondialdehyde (MDA), total sialic acid (TSA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels, which are known to be the markers of alcohol damage; and also (ii) caspase-3, tumor necrosis factor-alpha (TNF-α), and the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) as the markers of apoptosis. In the ethanol group, MDA, TSA, and TNF-α levels increased whereas SOD and CAT levels decreased compared with the control group. Ethanol+boric acid group MDA, TSA, caspase-3, and TNF-α levels decreased whereas SOD and CAT levels increased compared with the ethanol group. Using histopathological evaluation of light microscope images, immunohistochemical caspase-3 and TNF-α activity in the ethanol+boric acid group were shown to be decreased compared with that in the ethanol group. Our results revealed that ethanol is capable of triggering oxidative stress and apoptosis in the rat liver. We propose that boric acid is an effective compound in protecting the rat liver against ethanol.

Effects of pentoxifylline and platelet activating factor on sperm DNA damage.

OBJECTIVE: Pentoxifylline and platelet-activating factor (PAF) have been used to increase sperm motility in embryology laboratories. In the present study, we aimed to investigate whether these agents pose sperm DNA damage using DNA sperm chromatin dispersion (SCD) assay. STUDY DESIGN: Following application of pentoxifylline and PAF, sperm samples of 50 individuals with different sperm parameters were compared to baseline in terms of DNA damage using SCD assay. Furthermore, the relationship between DNA damage and sperm parameters in predicting DNA damage was assessed. RESULTS AND CONCLUSIONS: Significant increase in DNA damage was observed following application of PAF and pentoxifylline. Furthermore, DNA damage was significantly increased with application of pentoxifylline compared to PAF. Sperm motility was observed to be a statistically significant indicator in predicting alterations in DNA damage in baseline and subsequent to application of PAF and pentoxifylline independent of sperm concentration and morphology. Increased DNA damage was observed in both groups following application of pentoxifylline and PAF. Furthermore, the increase in DNA damage was higher in samples treated with pentoxifylline compared to samples treated with PAF. Thus, PAF seems to be more innocent in choosing viable sperm cells and in achieving sperm motility in the in vitro fertilization laboratory.

The impact of vessel clamps on endothelial integrity and function of saphenous vein grafts.

BACKGROUND: Saphenous vein graft (SVG) failure can be associated with endothelial damage during coronary artery bypass grafting (CABG). Endothelial damage may develop after application of occlusive vessel clamps on SVGs. This study was designed to investigate the effect of plastic and metal clamps on the endothelial integrity and function of SVGs. METHODS: Saphenous vein samples were obtained from 10 consecutive patients, who underwent an elective CABG using SVG. Plastic (group 1) and metal (group 2) clamps were sequentially applied on the vein. Each set of clamps (1 plastic and 1 metal) was removed and sampled at 5, 15, and 30 min, respectively. A short SVG segment was removed as control. The samples were fixed for histopathologic study using hematoxylin-eosin staining and immunostaining for endothelial nitric oxide synthase (eNOS) expression. In each group, endothelial, elastic tissue, muscular layer, and adventitial changes were investigated under light microscope and compared using a histologic scoring system. The intensity of eNOS expression was assessed using histochemical scoring system. RESULTS: In both groups, histopathologic examinations showed progressive endothelial damage in the zones of clamp application, compared with the control group (P<0.001). Histopathologic changes were more favorable with the metal clamps, compared with the plastic clamps, at 5 and 15 min. No significant increase in endothelial damage occurred after 15 min. The eNOS immunoreactivity of SVGs significantly decreased in the damaged areas of the endothelium (P<0.05). In metal clamps, the intensity of eNOS immunostaining was significantly high at 5 min, compared with plastic clamps (P<0.05). However, the intensity of eNOS expression in metal clamps was significantly lower than plastic clamps at 15 min (P<0.05). No significant difference was observed between the groups at 30 min. CONCLUSIONS: The endothelial cells can be better preserved with short-term application of SVGs with metal clamps rather than plastic clamps. These findings suggest that temporary use of metal clamps can be preferred without major effects on vascular integrity and function.

The effect of alpha-lipoic acid on NOS dispersion in the lung of streptozotocin-induced diabetic rats.

Oxidative stress and impaired bioactivity of nitric oxide (NO) play an important role in the organ pathogenesis and angiopathic complications of diabetes mellitus. In this study, we evaluated the effects of alpha-lipoic acid (ALA) on nitric oxide synthase (NOS) in lung tissues. ALA is a strong antioxidant. We wonder how it can affect oxidative stress and NO in the lung cells and vessels of diabetic rats. Wistar rats were divided into four groups; control, diabetic [65 mg/kg streptozotocin (STZ) for 15 days], STZ+ALA-treated (65 mg/kg ALA every 2 days for 15 days), and ALA-only-treated animals. At the end of the experimental period, lipid peroxidation, superoxide dismutase (SOD), and inducible NOS (iNOS) and endothelial NOS (eNOS) distribution were evaluated. Oxidative stress decreased with ALA in diabetic animals, and SOD also increased with ALA. iNOS and eNOS increased in diabetic animals, and ALA prevented iNOS increment in lung tissues. As a result, ALA can prevent some diabetic effects on the lungs and can also protect from vascular damages.

Inhibition of substance P activity prevents stress-induced bladder damage.

Substance P is a neuropeptide involved in inflammation, immune regulation and stress response. Stress may induce bladder damage by stimulating inflammatory response such as mast cell activation. We here examined the role substance P during stress-induced mast cell degranulation and urothelial injury in rat bladder. Adult Sprague-Dawley rats (200-270 g) were either exposed to cold-immobilization stress or substance P (SP) intracerebroventricularly. Different doses of substance P receptor (NK1R) antagonist CP 99994 were administered peripherally or centrally before the stress exposure. From each group, samples of the bladder were examined with light and electron microscope. Stress- and SP-injected centrally, increased the number of both granulated and degranulated mast cells. Ultrastructurally, urothelial degeneration with vacuolization in the cytoplasm and dilated intercellular spaces were seen. Both central and peripheral injection of CP 99994 prevented stress-induced urothelial degeneration as well as stress-induced mast cell degranulation. In conclusion, centrally and peripherally released substance P is involved in stress-induced bladder damage. Inhibition of NK1R prevents stress-induced pathological changes of urinary bladder and NK1R antagonist can be considered for the treatment of inflammatory bladder diseases.

Volume of nerve fibers in the stress-induced bladder of adult rats following capsaicin treatment.

INTRODUCTION: We have investigated the volume of nerve fibers in the rat urinary bladder following systematic exposure to cold-restraint stress and capsaicin treatment. MATERIALS AND METHODS: Adult Wistar albino rats were either exposed to cold-restraint stress (vehicle group) or treated with capsaicin before exposure to cold-restraint stress (capsaicin group). In the control group, animals were neither exposed to cold-restraint stress nor given capsaicin. From each group, samples of bladder were prepared for morphological investigation and stereological evaluation of the volume of nerve fibers. RESULTS: Stress exposure was associated with urothelial degeneration, a higher incidence and degranulation of mast cell profiles in the mucosa, and an increased volume of nerve fibers in the muscular layer of the bladder wall. Capsaicin treatment prevented the stress-induced degenerative changes. In the capsaicin group, the volume of nerve fibers in the muscular layer was also significantly smaller than that in the stress group. CONCLUSIONS: Exposure of adult rats to capsaicin prevented the stress-induced degeneration of the bladder and changed the volume of capsaicin-sensitive fibers in muscular layer. We conclude that capsaicin and related compounds may be useful in treating stress-induced bladder problems.