Abstract:Testicular dysfunction or damage is among the critical side effects of chemotherapeutic drugs like cisplatin. This study was mapped out to assess the possible therapeutic effect of eugenol on cisplatin‐induced testicular damage. In this experimental study, a single dose of cisplatin (15 mg/kg) was given intraperitoneally. After 72 hr of cisplatin injection, rats were sacrificed and testis tissues were removed. Tissues were examined by biochemical, histopathological and immunohistochemical methods. While tissue… Show more
“…A single dose of CISP (10 mg/kg, dissolved in 5 % DMSO/saline) was administered by intraperitoneal injection to the rats in the CISP and CISP+NRCE groups. The dose of CISP and NRCE were chosen based on previous literature [11,33] . After the last day of treatment, the rats were euthanized with sodium thiopental (150 mg/kg) and blood samples were obtained through cardiac puncture, centrifuged (3000 rpm for 15 min at 4 °C) to obtain the sera, which was subsequently used for the determination of testosterone and follicle stimulating hormone (FSH) levels.…”
Section: Methodsmentioning
confidence: 99%
“…The dose of CISP and NRCE were chosen based on previous literature. [11,33] After the last day of treatment, the rats were euthanized with sodium thiopental (150 mg/kg) and blood samples were obtained through cardiac puncture, centrifuged (3000 rpm for 15 min at 4°C) to obtain the sera, which was subsequently used for the determination of testosterone and follicle stimulating hormone (FSH) levels. The testes were rapidly excised, rinsed with normal saline and weighed.…”
Cisplatin (CISP) is an efficacious anticancer agent used in chemotherapy, however, the constraint to its clinical utility is the stray organ toxicity including testicular damage linked to oxidative and inflammatory cascades. This study aimed to explore the protective effect of nucleosides-rich extract from Cordyceps cicadae (NRCE) against CISP-induced testicular damage in rats. Rats were subjected to prophylactic oral administration of NRCE (50, 100 and 400 mg/kg body weight/day) for 7 days prior to testicular toxicity induced by CISP (10 mg/kg, ip) and were sacrificed after 72 h post-CISP injection. Cisplatin caused significant deficits in sperm count, viability and motility, testosterone and follicle stimulating hormone (FSH) compared to normal control. It depressed testicular activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), total antioxidant content (TAC), whereas malondialdehyde (MDA) increased remarkably. CISP considerably increased tumor necrosis factor-alpha (TNF-α) and interleukin-one beta (IL-1β) with alterations in testis histology compared to normal control. Interestingly, NRCE pretreatment inhibited the CISP-induced alterations in reproductive indices, restored the antioxidant activities in testes as well as inflammatory mediators and histology comparable to control. Our findings demonstrate that NRCE could prevent CISP testicular damage via inhibition of oxidative stress and proinflammation in rats.
“…A single dose of CISP (10 mg/kg, dissolved in 5 % DMSO/saline) was administered by intraperitoneal injection to the rats in the CISP and CISP+NRCE groups. The dose of CISP and NRCE were chosen based on previous literature [11,33] . After the last day of treatment, the rats were euthanized with sodium thiopental (150 mg/kg) and blood samples were obtained through cardiac puncture, centrifuged (3000 rpm for 15 min at 4 °C) to obtain the sera, which was subsequently used for the determination of testosterone and follicle stimulating hormone (FSH) levels.…”
Section: Methodsmentioning
confidence: 99%
“…The dose of CISP and NRCE were chosen based on previous literature. [11,33] After the last day of treatment, the rats were euthanized with sodium thiopental (150 mg/kg) and blood samples were obtained through cardiac puncture, centrifuged (3000 rpm for 15 min at 4°C) to obtain the sera, which was subsequently used for the determination of testosterone and follicle stimulating hormone (FSH) levels. The testes were rapidly excised, rinsed with normal saline and weighed.…”
Cisplatin (CISP) is an efficacious anticancer agent used in chemotherapy, however, the constraint to its clinical utility is the stray organ toxicity including testicular damage linked to oxidative and inflammatory cascades. This study aimed to explore the protective effect of nucleosides-rich extract from Cordyceps cicadae (NRCE) against CISP-induced testicular damage in rats. Rats were subjected to prophylactic oral administration of NRCE (50, 100 and 400 mg/kg body weight/day) for 7 days prior to testicular toxicity induced by CISP (10 mg/kg, ip) and were sacrificed after 72 h post-CISP injection. Cisplatin caused significant deficits in sperm count, viability and motility, testosterone and follicle stimulating hormone (FSH) compared to normal control. It depressed testicular activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), total antioxidant content (TAC), whereas malondialdehyde (MDA) increased remarkably. CISP considerably increased tumor necrosis factor-alpha (TNF-α) and interleukin-one beta (IL-1β) with alterations in testis histology compared to normal control. Interestingly, NRCE pretreatment inhibited the CISP-induced alterations in reproductive indices, restored the antioxidant activities in testes as well as inflammatory mediators and histology comparable to control. Our findings demonstrate that NRCE could prevent CISP testicular damage via inhibition of oxidative stress and proinflammation in rats.
“…Eugenol is one of active compounds of a well-known traditional Chinese medicine Acorus gramineus, which has attracted wide attention for its antiinflammatory (El-Kady et al, 2019), antiapoptotic (Ekinci Akdemir et al, 2019), antioxidant (Ekinci Akdemir et al, 2019), and antitumor (Fangjun and Zhijia, 2018) effects. A previous study showed that eugenol could protect against hepatic ischemia-reperfusion injury (Abd El Motteleb et al, 2014).…”
Eugenol, as an active compound isolated from Acorus gramineus, has been shown to protect against cerebral ischemia-reperfusion (I/R) injury. Nonetheless, the detailed neuroprotective mechanisms of eugenol in cerebral I/R injury have not been elaborated. In the present study, cerebral I/R injury model was established by middle cerebral artery occlusion (MCAO) in rats. HT22 cells were subjected to oxygen-glucose deprivation/ reperfusion (OGD/R) to mimic cerebral I/R injury in vitro. The results showed that eugenol pre-treatment relieved cerebral I/R injury as evidenced by improving neurological deficits and reducing infarct volume. Autophagy was induced by MCAO, which was further promoted by eugenol administration. Moreover, rapamycin, an activator of autophagy, promoted eugenol-induced decreases in neurological score, infarct volume, brain water content, and apoptosis. However, pretreatment with 3-MA, an inhibitor of autophagy, led to the opposite results. Similarly, eugenol pretreatment increased the viability and restrained apoptosis of OGD/R-challenged HT22 cells. OGD/R-induced autophagy was strengthened by eugenol. Mechanically, eugenol promoted autophagy through regulating AMPK/mTOR/P70S6K signaling pathway in vivo and in vitro. In conclusion, pretreatment with eugenol attenuated cerebral I/R injury by inducing autophagy via AMPK/mTOR/ P70S6K signaling pathway.
“…Testicular oxidative stress has been reported to be detrimental to male fertility health (Turner & Lysiak, 2008; Yesil et al., 2018). The use of exogenous antioxidants such as eugenol (Table 1) have been reported to improve testicular dysfunctions (Aitken & Roman, 2009; Ekinci akdemir et al., 2019; Imam et al., 2017). The ability of the infusion to restore the testicular antioxidant capacity indicates a potent protective effect against oxidative testicular injury, which may be attributed to its phenolic content.…”
Oxidative stress is a primary culprit in the pathophysiology of infertility conditions in males. This study investigated the effects of Ocimum tenuiflorum on redox imbalance, cholinergic and purinergic dysfunctions and glucose dysmetabolism in oxidative‐mediated testicular toxicity using in vitro, ex vivo and in silico models. Induction of oxidative testicular injury was carried out by incubating normal testicular tissue with 0.1 mM FeSO4 and treated by co‐incubating with different concentrations of O. tenuiflorum infusion for 30 min at 37°C. O. tenuiflorum displayed significant ferric reducing power activity while scavenging DPPH and hydroxyl (OH˙) free radicals in vitro. Oxidative testicular injury significantly reduced the glutathione level and superoxide dismutase and catalase activities with concomitant elevation of malondialdehyde and nitric oxide levels and acetylcholinesterase, ATPase, fructose‐1,6‐bisphosphatase and glycogen phosphorylase (GlyP) activities. Incubation with the infusion significantly reversed these levels and activities. The phytochemical constituent of the infusion was detected by gas chromatography–mass spectroscopy analysis and revealed favourable binding energies when docked with some of the studied proteins. These results suggest O. tenuiflorum exerts a protective effect against Fe2+ induced testicular toxicity via mitigation of redox imbalance while modulating metabolic dysfunctions linked to male infertility.
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