The effect of ghrelin pretreatment on epididymal sperm quality and tissue antioxidant enzyme activities after testicular ischemia/reperfusion in rats
Ghrelin, the endogenous ligand for growth hormone secretagogue receptor, has been reported to prevent ischemia/reperfusion (I/R) injury in various tissues by its antioxidant activity. Therefore, this study was aimed to investigate the effect of ghrelin on sperm quality and antioxidant enzyme activity in a rat testicular ischemia/reperfusion injury model. Forty-two male Wistar rats were divided into groups control, I/R, and I/R plus ghrelin. The right testes were rotated 720° for 1 h and were allowed to reperfuse for 4 h and 30 days thereafter. Ghrelin (40 nmol/kg IP) or vehicle (physiological saline) was administrated 15 min before reperfusion. After 4 h of reperfusion, a right orchiectomy was performed to measure the biochemical parameters. In addition, the sperm was collected from the epididymis after 30 days of reperfusion, and sperm characteristics were examined. The malondialdehyde levels of the testis tissues were significantly increased, but a statistically significant decrease was found in the superoxide dismutase, glutathione peroxidase, and catalase activities in the I/R group as compared with the control, indicating I/R injury. The sperm evaluation showed a significant reduction in all characteristics resulted from I/R compared with the control. In the ghrelin-treated group, the malondialdehyde values were significantly lowered, and only enzyme activity of glutathione peroxidase showed significant increases compared with the I/R group. Ghrelin significantly enhanced sperm motility, movement, and concentration but did not prevent I/R-induced reduction in membrane integrity in the testes of rats compared to the I/R group. Our results suggest that ghrelin treatment has a protective role on IR-induced testicular injury, and this effect may be due to its antioxidant properties.
Available from: Natale Figura
- "These observations suggest that ghrelin could regulate spermatogenesis in an autocrine and/or paracrine manner, also because there is evidence that ghrelin is able to modulate testicular key functions, such as seminiferous tubule gene expression, testosterone secretion and Leydig cells proliferation (Dupont et al., 2010). In addition, it was demonstrated in rat that ghrelin, localised in Leydig and Sertoli cells (Barreiro et al., 2002; Garc ıa et al., 2007; Dupont et al., 2010), is endowed with antioxidant properties (Kheradmand et al., 2009; Taati et al., 2012), role that deserves attention and could be explored in humans. "
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ABSTRACT: The role of ghrelin and obestatin in male reproduction has not completely been clarified. We explored ghrelin and obestatin localisation in the male reproductive system. Polyclonal antibodies anti-ghrelin and anti-obestatin were used to detect the expression of these hormones in human testis, prostate and seminal vesicles by immunocytochemistry, while in ejaculated and swim up selected spermatozoa by immunofluorescence. Sertoli cells were positive for both peptides and Leydig cells for ghrelin; germ cells were negative for both hormones. Mild signals for ghrelin and obestatin were observed in rete testis; efferent ductules were the most immune reactive region for both peptides. Epididymis was moderately positive for ghrelin; vas deferens and seminal vesicles showed intense obestatin and moderate ghrelin labelling; prostate tissue expressed obestatin alone. Ejaculated and selected spermatozoa were positive for both peptides in different head and tail regions. This study confirms ghrelin localisation in Leydig and Sertoli cells; the finding that ghrelin is expressed in rete testis, epididymis, vas deferens and seminal vesicles is novel, as well as the localisation of obestatin in almost all tracts of the male reproductive system. This research could offer insights for stimulating other studies, particularly on the role of obestatin in sperm physiology, which is still obscure.
Available from: Alireza Sarkaki
- "The antioxidant defense mechanisms include antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and several non-enzymatic free radical scavengers (Murray and Stein 1989; Simon et al., 1984). The nervous tissue has a high content of polyunsaturated fatty acids (Sun et al., 2002), which are easy targets to oxidative damage by free radicals due to the unsaturated bonds they contain (Taati et al., 2012). On the other hand, it has been revealed that brain structures such as hippocampus which support memory are uniquely sensitive to oxidative stress due to their elevated demand for oxygen (Urso and Clarkson, 2003; Vannucci and Vannucci, 1997; Wickens 2001). "
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ABSTRACT: Objective: It is generally agreed that most of the phenomena observed during brain ischemia and reperfusion can be explained by the damage to membrane structure. Oxidative stress is resulted in an imbalance between high consumption of oxygen and low levels of endogenous antioxidants. It is known that gallic acid (GA) is a strong antioxidant. The present study was carried out to evaluate the effect of GA on ischemia/reperfusion (I/R)-induced brain injury in rats.
Methods: Wistar adult male rats weighing 200–250 g were divided into six groups as sham operated (Sh), ischemia/reperfusion (I/R) received normal saline (I+Veh), I/R groups treated with gallic acid (I+GA, 50, 100, or 200 mg/kg, orally, respectively), or with 100 mg /kg phenytoin (I+Phen). The global cerebral I/R injury was induced by occluding bilateral common carotid arteries (BCCA) for 20 min, followed by 5 days reperfusion in adult male rats.
Results: It was found that administration of 100 mg/kg GA for 5 days before and 5 days after I/R induction reversed gait performance, sensorimotor disorders (p<0.01), and hypoalgesia (p<0.001) while dose of 50 mg/kg increased passive avoidance memory significantly (p<0.05).
Conclusion: Our findings clearly demonstrate that GA has beneficial effects on behavioral impairments after brain injury induced by I/R. The results of this study show that GA pretreatment ameliorates cerebral ischemia/reperfusion injury and enhances the antioxidant defense against BCCA occlusion-induced I/R in rats, so it exhibits cerebroprotective property.
Available from: Maryam Rafieirad
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ABSTRACT: This study aimed to evaluate the effect of two weeks oral administration of pomegranate seed extract (PGSE) on active and passive avoidance memories after permanent bilateral common carotid arteries occlusion (2CCAO) to induce permanent cerebral ischemia in adult female rats.
Seventy adult female Wistar rats (250 ± 20 g) were used. Animals were divided randomly into seven groups with 10 in each: 1) Sham-operated; 2) Ischemic; 3-6) Ischemic received PGSE (100, 200, 400, and 800 mg/2mL/kg, orally) for 14 days; 7) Ischemic received vehicle. In order to create 2CCAO, carotid arteries were ligatured and then cut bilaterally. Active and passive avoidance task were measured using criterion condition responses (CCRs) in Y-maze and step-through latency (STL) in two-way shuttle box in all female rats.
Both active and passive avoidance memories were significantly impaired in rats after cerebral hypoxia-ischemia (CHI) (P < 0.001). PGSE treatment significantly improved passive and active memory impairments with 2CCAO (P < 0.05, P < 0.01, and P < 0.001). No toxicity was observed even with high-dose PGSE consumption (800 mg/kg, for 14 days).
PGSE exhibits therapeutic potential for avoidance memories, which is most likely related at least in part to its antioxidative and free radical scavenging actions.
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