scholarly journals The Potential Protective Effect and Possible Mechanism of Peptides from Oyster (Crassostrea hongkongensis) Hydrolysate on Triptolide-Induced Testis Injury in Male Mice

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 566
Author(s):  
Xueyan Zhang ◽  
Zhilan Peng ◽  
Huina Zheng ◽  
Chaohua Zhang ◽  
Haisheng Lin ◽  
...  
Keyword(s):  
Protective Effect ◽  
Antioxidant Enzyme ◽  
Sperm Count ◽  
Biological Activities ◽  
Regulatory Protein ◽  
Underlying Mechanism ◽  
Male Reproduction ◽  
Injury Model ◽  
Serum Hormone ◽  
Testicular Injury

Peptides from oyster hydrolysate (OPs) have a variety of biological activities. However, its protective effect and exact mechanism on testicular injury remain poorly understood. This study aimed to evaluate the protective effect of OPs on triptolide (TP)-induced testis damage and spermatogenesis dysfunction and investigate its underlying mechanism. In this work, the TP-induced testis injury model was created while OPs were gavaged in mice for 4 weeks. The results showed that OPs significantly improved the sperm count and motility of mice, and alleviated the seminiferous tubule injury. Further study showed that OPs decreased malonaldehyde (MDA) level and increased antioxidant enzyme (SOD and GPH-Px) activities, attenuating oxidative stress and thereby reducing the number of apoptotic cells in the testis. In addition, OPs improved the activities of enzymes (LDH, ALP and ACP) related to energy metabolism in the testis and restored the serum hormone level of mice to normal. Furthermore, OPs promoted the expression of Nrf2 protein, and then increased the expression of antioxidant enzyme regulatory protein (HO-1 and NQO1) in the testis. OPs inhibited JNK phosphorylation and Bcl-2/Bax-mediated apoptosis. In conclusion, OPs have a protective effect on testicular injury and spermatogenesis disorders caused by TP, suggesting the potential protection of OPs on male reproduction.

Effect of visnagin on altered steroidogenesis and spermatogenesis, and testicular injury induced by the heavy metal lead

2020 ◽  
Vol 23 ◽  
Author(s):  
Jamaan S. Ajarem ◽  
Ahmad K. Hegazy ◽  
Gamal A. Allam ◽  
Ahmed A. Allam ◽  
Saleh N. Maodaa ◽  
...  
Keyword(s):  
Protective Effect ◽  
Sperm Count ◽  
Protective Efficacy ◽  
Reproductive Toxicity ◽  
Serum Levels ◽  
Environmental Pollutant ◽  
Promising Candidate ◽  
Sperm Abnormalities ◽  
Testicular Injury ◽  
Pro Inflammatory Cytokines

Background: Lead (Pb) is an environmental pollutant causing serious health problems, including impairment of reproduction. Visnagin (VIS) is a furanochromone with promising antioxidant and anti-inflammatory effects; however, its protective efficacy against Pb toxicity has not been investigated. Objective: This study evaluated the protective effect of VIS on Pb reproductive toxicity, impaired steroidogenesis and spermatogenesis, oxidative stress and inflammation. Methods: Rats received VIS (30 or 60 mg/kg) and 50 mg/kg lead acetate for 3 weeks and blood and testes samples were collected. Results: Pb intoxication impaired the pituitary-testicular axis (PTA) manifested by the decreased serum levels of gonadotropins and testosterone. Pb decreased sperm count, motility and viability, increased sperm abnormalities, and downregulated the steroidogenesis markers StAR, CYP17A1, 3β-HSD and 17β-HSD in the testis of rats. VIS significantly increased serum gonadotropins and testosterone, alleviated sperm parameters and upregulated steroidogenesis. In addition, VIS decreased pro-inflammatory cytokines, testicular lipid peroxidation and DNA fragmentation, downregulated Bax, and enhanced antioxidants and Bcl-2. Conclusion: These results demonstrate the protective effect of VIS against Pb reproductive toxicity in rats. VIS improved serum gonadotropins and testosterone, enhanced steroidogenesis and spermatogenesis, and attenuated oxidative injury, inflammation and apoptosis. Therefore, VIS is a promising candidate for the protection against Pb-induced reproduction impairment.

The Protective Effect of Metformin against Oxandrolone-Induced Infertility in Male Rats

2020 ◽  
Vol 26 ◽  
Author(s):  
Abdulqader Fadhil Abed ◽  
Yazun Bashir Jarrar ◽  
Hamzeh J Al-Ameer ◽  
Wajdy Al-Awaida ◽  
Su-Jun Lee
Keyword(s):  
Gene Expression ◽  
Male Infertility ◽  
Protective Effect ◽  
Histological Examination ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Male Rats ◽  
P Value ◽  
Protective Effects ◽  
Rt Pcr

Background: Oxandrolone is a synthetic testosterone analogue that is widely used among bodybuilders and athletes. However, oxandrolone causes male infertility. Recently, it was found that metformin reduces the risk of infertility associated with diabetes mellitus. Aim: This study aimed to investigate the protective effects of metformin against oxandrolone-induced infertility in male rats. Methods: Rats continuously received one of four treatments (n=7) over 14 days: control DMSO administration, oxandrolone administration, metformin administration, or co-administration of oxandrolone and metformin. Doses were equivalent to those used for human treatment. Subsequently, testicular and blood samples were collected for morphological, biochemical, and histological examination. In addition, gene expression of the testosterone synthesizing enzyme CYP11A1 was analyzed in the testes using RT-PCR. Results: Oxandrolone administration induced male infertility by significantly reducing relative weights of testes by 48%, sperm count by 82%, and serum testosterone levels by 96% (ANOVA, P value < 0.05). In addition, histological examination determined that oxandrolone caused spermatogenic arrest which was associated with 2-fold downregulation of testicular CYP11A1 gene expression. However, co-administration of metformin with oxandrolone significantly ameliorated toxicological alterations induced by oxandrolone exposure (ANOVA, P value < 0.05). Conclusion: Metformin administration protected against oxandrolone-induced infertility in male rats. Further clinical studies are needed to confirm the protective effect of metformin against oxandrolone-induced infertility among athletes.

scholarly journals Protective effect of snail secretion filtrate against ethanol-induced gastric ulcer in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Enrico Gugliandolo ◽  
Marika Cordaro ◽  
Roberta Fusco ◽  
Alessio Filippo Peritore ◽  
Rosalba Siracusa ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Underlying Mechanism ◽  
New Drugs ◽  
Ethanol Administration ◽  
Common Disease ◽  
Intragastric Administration ◽  
Human Disorders ◽  
Interest In Research

AbstractGastric ulcer or peptic ulcer is a common disease worldwide. Basically, it develops when there is an imbalance between the protective and aggressive factors, especially at the luminal surface of epithelial cells. Thus, there is a constant interest in research new drugs for treatment of gastric ulcer. The snail secretion is a dense mucous, that covers the external surface of the snails, with important functions for the survival of snails. The biological proprieties of snail Helix Aspersa Muller mucus it has been known for centuries to treat human disorders in particular for skin disease. Recently the use of snail mucus has seen a worldwide increase, as a component in cosmetic product and it has been used in particular for the management of wound and skin disorders. In this study we use a murine model of ethanol intragastric administration which has been widely used to test the drugs efficacies and to explore the underlying mechanism for gastric ulcer development. The intragastric ethanol administration causes several mucosal damages and an induction of a severe inflammatory response. Our results show a significant protective effect of snail secretion filtrate in reducing macroscopic and histological lesions, as well the protective effect on mucus content, oxidative stress and inflammatory response. In conclusion this study demonstrate the protective effect of intragastrical snail secretion filtrate, in a model of ethanol-induced gastric ulcer in mice, suggesting its possible useful use in the treatment or prevention of gastric ulcer.

scholarly journals SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhiya Deng ◽  
Maomao Sun ◽  
Jie Wu ◽  
Haihong Fang ◽  
Shumin Cai ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Cell Model ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Autophagy Induction ◽  
Promising Therapeutic Approach ◽  
Related Proteins ◽  
Caecal Ligation And Puncture

AbstractOur previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.

scholarly journals The Protective Effect of Total Flavones from Rhododendron simsii Planch. on Myocardial Ischemia/Reperfusion Injury and Its Underlying Mechanism

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Sheng-Yong Luo ◽  
Qing-Hua Xu ◽  
Gong Peng ◽  
Zhi-Wu Chen
Keyword(s):  
Myocardial Infarction ◽  
Protective Effect ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Assay Method ◽  
Protective Effects ◽  
Rhododendron Simsii ◽  
Rhoa Activity ◽  
Protein Expressions

Objectives. Total flavones from Rhododendron simsii Planch. (TFR) are the effective part extracted from the flowers of Rhododendron simsii Planch. and have obvious protective effects against cerebral ischemic or myocardial injuries in rabbits and rats. However, their mechanism of cardioprotection is still unrevealed. Therefore, the present study was designed to investigate the effect of TFR on myocardial I/R injury and the underlying mechanism. Methods. TFR groups were treated by gavage once a day for 3 days at a dose of 20, 40, and 80 mg/kg, respectively, and then the model of myocardial I/R injury was established. Myocardial infarction, ST-segment elevation, and the expression of UTR, ROCK1, ROCK2, and p-MLC protein in rat myocardium were determined at 90 min after reperfusion. UTR siRNA in vivo transfection and competition binding assay method were used to study the relationship between the protective effect of TFR and UTR. Results. The expression of UTR protein markedly decreased in myocardium of UTR siRNA transfection group rats. TFR could significantly reduce the infarct size and inhibit the increase of RhoA activity and ROCK1, ROCK2, and p-MLC protein expressions both in WT and UTR knockdown rats. The reducing rate of TFR in myocardial infarction area, RhoA activity, and ROCK1, ROCK2, and p-MLC protein expressions in UTR knockdown rats decreased markedly compared with that in WT rats. In addition, TFR had no obvious effect on the increase of ΣST in UTR knockdown rats in comparison with that in model group. In particular, TFR could significantly inhibit the combination of [I125]-hu-II and UTR, and IC50 was 0.854 mg/l. Conclusions. The results indicate that the protective effect of TFR on I/R injury may be correlated with its blocking UTR and the subsequent inhibition of RhoA/ROCK signaling pathway.

scholarly journals Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation

2017 ◽  
Vol 313 (4) ◽  
pp. L710-L721 ◽  
Author(s):  
Yunbo Ke ◽  
Olga V. Oskolkova ◽  
Nicolene Sarich ◽  
Yufeng Tian ◽  
Albert Sitikov ◽  
...  
Keyword(s):  
Protective Effect ◽  
Vascular Endothelial Cells ◽  
Biological Activities ◽  
Cell Monolayer ◽  
Endothelial Permeability ◽  
In Vivo Model ◽  
Barrier Dysfunction ◽  
Anti Inflammatory

Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory effects of PGE2 and PGI2 on vascular endothelial cells (EC). Yet, the effects of other PG members on EC barrier and inflammatory activation have not been systematically analyzed. This study compared effects of PGE2, PGI2, PGF2α, PGA2, PGJ2, and PGD2 on human pulmonary EC. EC permeability was assessed by measurements of transendothelial electrical resistance and cell monolayer permeability for FITC-labeled tracer. Anti-inflammatory effects of PGs were evaluated by analysis of expression of adhesion molecule ICAM1 and secretion of soluble ICAM1 and cytokines by EC. PGE2, PGI2, and PGA2 exhibited the most potent barrier-enhancing effects and most efficient attenuation of thrombin-induced EC permeability and contractile response, whereas PGI2 effectively suppressed thrombin-induced permeability but was less efficient in the attenuation of prolonged EC hyperpermeability caused by interleukin-6 or bacterial wall lipopolysaccharide, LPS. PGD2 showed a modest protective effect on the EC inflammatory response, whereas PGF2α and PGJ2 were without effect on agonist-induced EC barrier dysfunction. In vivo, PGE2, PGI2, and PGA2 attenuated LPS-induced lung inflammation, whereas PGF2α and PGJ2 were without effect. Interestingly, PGD2 exhibited a protective effect in the in vivo model of LPS-induced lung injury. This study provides a comprehensive analysis of barrier-protective and anti-inflammatory effects of different prostaglandins on lung EC in vitro and in vivo and identifies PGE2, PGI2, and PGA2 as prostaglandins with the most potent protective properties.

scholarly journals Determination of in Vivo Biological Activities of Dodonaea Viscosa Flowers Against CCL4 Toxicity in Albino Mice With Bioactive Compound Detection

2021 ◽  
Author(s):  
Hina Gul ◽  
Muhammad Awais ◽  
Salina Saddick ◽  
Falak Sher Khan ◽  
Muhammad Gulfraz ◽  
...  
Keyword(s):  
Protective Effect ◽  
Biological Activities ◽  
Hematological Parameters ◽  
Octadecenoic Acid ◽  
Radical Scavenging ◽  
Herbal Medicines ◽  
Bioactive Compound ◽  
Dodonaea Viscosa

Abstract Dodonaea viscosa L. Jacq. is an evergreen shrub and native to Asia, Africa and Australia. It has been used as traditional medicine in different countries. The foremost objective of the current study was to discover protective potential of D. Viscosa flowers Methanol (DVM) and Chloroform (DVC) extracts against CCL4 induced toxicity in mice. This study was intended to identify phytochemicals through HPLC, GCMS and FT-IR as well as in vitro antioxidant and in vitro antituberculosis activity. Our comprehensive findings indicate that Dodonaea viscosa is valuable and widespread herbal medicines through therapeutic potentials for curing various ailments. Dodonaea viscosa flowers are found to have protective effect against oxidative stress produced by CCL4 in liver, kidney and spleen. The level of hepatic enzymes (ALP, AST ALT and Direct bilirubin), hematological parameters (RBCs, WBCs and Platelets), total protein and liver antioxidant enzymes (SOD, GPx and CAT) were restored by the intake of DV extracts after decline in levels by CCL4. Histopathological results discovered the defensive effect of 300mg/kg of DVM extract against CCL4 induced damage, thus having improved protective effect as compared to DVC and control. As a result of analysis total flavonoids and total phenolics were also revealed. Phytochemical investigation by HPLC identified gallic acid, epicatechin, cumeric acid, flavonoids while Oleic acid (Octadecenoic acid) (C18H34O2), Stearic acid (C18H36O2), Ricinoleic acid (C18H34O3) and Cedrol (C15H26O) was estimated by GCMS. DVM extract exhibited resistance against in vitro Mycobacterium tuberculosis strains. This study proposed that protective effect of DV against oxidative damage induced in Liver, Kidney and Spleen can possibly be correlated to their antioxidant as well as free radical scavenging property.

scholarly journals What Is the Impact of Excessive Iodine and Semen Quality in Fertile Men of China: An Association Study 

2021 ◽  
Author(s):  
Ning Wang ◽  
Fang Lv ◽  
Ge Yu ◽  
Cuige Shi ◽  
Shangming Wang ◽  
...  
Keyword(s):  
Semen Quality ◽  
Sperm Count ◽  
Sperm Concentration ◽  
Urinary Iodine ◽  
Iodine Concentration ◽  
Male Reproduction ◽  
Semen Parameters ◽  
Human Thyroid ◽  
Urinary Iodine Concentration ◽  
The Impact

Abstract Background: Iodine is an essential element for hormones synthesized by the human thyroid gland. Thyroid hormone deficiency affects all body tissues, including multiple endocrine changes that alter growth hormones, corticotrophin, glucocorticoids, and gonadal function. In many countries, subfertility is an important problem affecting about 10–15% of all couples trying to conceive. Male subfertile factors have accounted for 25–30% of all cases in their studies. The aim of this study was to study the correlation between urinary iodine concentration (UIC) and semen quality of fertile male in China.Methods: semen and urine samples were collected from males who attended a survey for the reproductive physiological constants of male and female in China. All participants were fertile and they should be free from diseases of male reproductive system and thyroid related diseases. We studied the correlation between UIC and semen quality parameters in fertile males and the effect of iodine concentration on male reproduction. Participants were divided into six groups based on UIC. We measured semen parameters and UIC. Semen parameters or time-to-pregnancy (TTP) were analyzed by Spearman correlation, linear regression and multivariable logistic regression. Results: 1089 men were recruited in the study. The mean and median age of participants were 27.46±0.12 and 27±3.88 years, respectively. UIC of 274 (25.16%) men was lower than the UIC of WHO recommended. UIC of 405 men located in the region of WHO recommended. 62.35% of them were not located in the optimal region. Semen concentration and total sperm count were found to decrease when UIC increases when the UIC≥100 ug/L. Conclusions: A male with deficient UIC or excessive UIC has more risk of lower semen quality such as sperm concentration and total sperm count. In addition, if a male with deficient UIC or excessive UIC, his wife has longer TTP than the males who had normal UIC. Deficient UIC associated with lower semen quality and TTP than excessive UIC.

scholarly journals Hydrogen Sulfide Protects Cardiomyocytes against Apoptosis in Ischemia/Reperfusion through MiR-1-Regulated Histone Deacetylase 4 Pathway

2016 ◽  
Vol 41 (1) ◽  
pp. 10-21 ◽  
Author(s):  
Bo Kang ◽  
Wei Li ◽  
Wang Xi ◽  
Yinghong Yi ◽  
Yundan Ciren ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tumor Cells ◽  
Histone Deacetylase ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Neonatal Rats ◽  
Histone Deacetylase 4

Background/Aims: Hydrogen sulfide (H<Sub>2</Sub>S) is a powerful inhibitor of cardiomyocytes apoptosis following ischemia/reperfusion (IR) injury, but the underlying mechanism remains unclear. Our previous study showed that microRNA-1 (miR-1) was upregulated by 2.21 fold in the IR group compared with that in the H<Sub>2</Sub>S preconditioned group. MiR-206 affected the process of cardiomyocytes hypertrophy by regulating histone deacetylase 4 (HDAC4). HDAC4 is also known to play an anti-apoptotic role in tumor cells, but its role in the myocardium has not been reported. The aim of this study was to test whether H<Sub>2</Sub>S could inhibit apoptosis of cardiomyocytes through HDAC4 regulation by miR-1 in IR. Methods: Cardiomyocytes of neonatal rats were subjected to hypoxia/reoxygenation (HR) injury with or without H<Sub>2</Sub>S pretreatment to simulate IR injury Cardiomyocytes were transfected with miR-1 mimic or HDAC4 siRNA to evaluate whether the miR-1-HDAC4 signaling pathway was involved in the protective effect of H<Sub>2</Sub>S. Results: HR increased cell apoptosis and caspase-3 cleavage, upregulated miR-1, and downregulated HDAC4. H<Sub>2</Sub>S preconditioning attenuated the apoptosis of cardiomyocytes, caspase-3 cleavage and LDH release, and enhanced cell viability In addition, H<Sub>2</Sub>S downregulated miR-1, and preserved HDAC4 expression. HDAC4 protein was down-regulated by miR-1 mimic. Transfection of cardiomyocytes with miR-1 mimic partially reduced the protective effect of H<Sub>2</Sub>S. Meanwhile, transfection of cardiomyocytes with siRNA to HDAC4 partially abrogated the protective effect of H<Sub>2</Sub>S. Conclusions: The miR-1-HDAC4 signaling pathway is involved in the protective effect of H<Sub>2</Sub>S against the apoptosis of cardiomyocytes during the IR injury process.

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