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1.
Anatomy & Cell Biology ; : 183-190, 2019.
Article in English | WPRIM | ID: wpr-762214

ABSTRACT

Nicotine is the most toxic factor of tobacco. Genistein is a phytoestrogen and antioxidant that has numerous health benefits. The aim of this study is to evaluate the effects of genistein against toxic properties of nicotine to the pancreas of mice. For this purpose, 48 male mice were randomly assigned into six groups (n=8): normal control, nicotine control (2.5 mg/kg), genistein (25 and 50 mg/kg), and nicotine+genistein (25 and 50 mg/kg) treated groups. Various doses of genistein and genistein+nicotine were administered intraperitoneally to animals for 4 weeks. The weight of pancreas, total antioxidant capacity and nitrite oxide of serum, insulin levels, and the number and diameter of islets of Langerhans were investigated. Nicotine administration reduced significantly total antioxidant capacity, insulin, pancreas weight, and the number and diameter of islets of Langerhans and increased nitrite oxide in serum compared to the control normal group (P<0.05). Conversely, genistein and genistein+nicotine increased significantly insulin, total antioxidant capacity, and the number and diameter islets of Langerhans and decreased serum nitrite oxide compared to the nicotine control group. It seems that the genistein can improve pancreas damage following the nicotine administration.


Subject(s)
Animals , Humans , Male , Mice , Genistein , Insulin , Insurance Benefits , Islets of Langerhans , Nicotine , Pancreas , Phytoestrogens , Nicotiana
2.
Asian Pacific Journal of Tropical Biomedicine ; (12): 150-157, 2019.
Article in Chinese | WPRIM | ID: wpr-744060

ABSTRACT

Objective: To assess the effects of Falcaria vulgaris (F. vulgaris) as an antioxidant on damage to kidney of diabetic rats.Methods: Diabetic rats were established via streptozotocin (60 mg/kg). Various doses of F. vulgaris extracts (50, 100 and 150 mg/kg) and streptozotocin + F. vulgaris extracts were administered via intraperitoneal (i.p) injection to 48 rats (n=8 per group) for 28 d.Subsequently, ferric ion reducing antioxidant power (FRAP) of renal tissue, thiobarbituric acid reactive species, blood glucose concentrations, insulin, nitrite oxide, the weight of animals,glomeruli characteristics and kidney function were evaluated.Results: Compared with the control rats, diabetic rats showed significant increase in malondialdehyde, blood urea nitrogen, creatinine, blood glucose, nitrite oxide contents in renal tissues, and glomerular diameter. Furthermore, tissue FRAP level, body weight, number of glomeruli and plasma insulin were markedly reduced in diabetic rats when compared with the control group (P < 0.05). However, in all F. vulgaris and F. vulgaris + streptozotocin groups,malondialdehyde level, blood urea nitrogen, creatinine, glomerular diameter, nitrite oxide,and glucose levels were decreased significantly; meanwhile, tissue FRAP level, body weight,glomeruli number and insulin serum level were increased, compared to the control diabetic group (P < 0.05).Conclusions: F. vulgaris extract alleviates renal damage in diabetic rats.

3.
Chinese Medical Journal ; (24): 1598-1604, 2018.
Article in English | WPRIM | ID: wpr-688072

ABSTRACT

<p><b>Background</b>Morphine is commonly used to treat severe pain. This substance is significantly metabolized in the liver and causes disturbing effects. Genistein is an isoflavone and has antioxidant properties. The aim of this study was to evaluate the effects of genistein against morphine damages on mouse liver.</p><p><b>Methods</b>Between May 2017 and March 2018, 48 male mice were divided into six groups (n = 8 in each group). Various doses of genistein (25 and 50 mg/kg) and morphine plus genistein (25 and 50 mg/kg) were administered intraperitoneally to 48 male mice for 20 consequent days. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), serum nitric oxide (NO) levels, liver weight, and the diameter of hepatocytes and central hepatic vein were studied and compared using one-way analysis of variance.</p><p><b>Results</b>Morphine administration significantly increased the mean diameter of the central hepatic vein (22.76 ± 1.9 μm vs. 15.04 ± 0.60 μm, χ = 21.814, P = 0.001) and hepatocytes (3.03 ± 0.10 μm vs. 1.10 ± 0.05 μm, χ = 9.873, P = 0.001) respectively, blood serum NO level (38.00% ± 2.09% vs. 18.72% ± 4.40%, χ = 20.404, P < 0.001), liver enzyme level (AST: 111.80 ± 5.10 ng/ml vs. 81.93 ± 2.20 ng/ml, χ = 32.201, P < 0.0001; ALT: 45.14 ± 4.10 ng/ml vs. 35.49 ± 2.50 ng/ml, χ = 18.203, P < 0.0001; and ALP: 3.28 ± 0.20 ng/ml vs. 2.14 ± 0.10, χ = 5.04, P < 0.0001, respectively), and decreased liver weight (18.50 ± 0.90 g vs. 27.15 ± 0.50 g, χ = 22.415, P = 0.001) compared to saline group (0.535-0.750, P < 0.0001). However, administration of genistein plus morphine significantly enhanced liver weight (25 mg/kg: 21.15 ± 2.13 g vs. 18.50 ± 0.90 g, χ = 19.251, P < 0.0001; 50 mg/kg: 21.20 ± 1.00 g vs. 18.5 ± 0.9 g, χ = 19.502, P < 0.0001, respectively) and reduced the mean diameter of hepatocyte (25 mg/kg: 2.17 ± 0.30 μm vs. 3.03 ± 0.10 μm, χ = 22.780, P = 0.001; 50 mg/kg: 2.01 ± 0.20 μm vs. 3.03 ± 0.10 μm χ = 7.120, P = 0.001, respectively), central hepatic vein (25 mg/kg: 19.53 ± 1.00 μm vs. 22.76 ± 1.90 μm, χ = 20.681, P = 0.001; 50 mg/kg: 19.44 ± 1.20 μm vs. 22.76 ± 1.90 μm, χ = 18.451, P = 0.001, respectively), AST (25 mg/kg: 95.40 ± 5.20 ng/ml vs. 111.80 ± 5.010 ng/ml, P < 0.0001; 50 mg/kg: 90.78 ± 6.00 ng/ml vs. 111.80 ± 5.10 ng/ml, χ = 17.112, P < 0.0001, respectively), ALT (25 mg/kg: 35.78 ± 5.01 ng/ml vs. 45.14 ± 4.10 ng/ml, χ = 15.320, P < 0.0001; 50 mg/kg: 33.78 ± 2.60 ng/ml vs. 45.14 ± 4.10 ng/ml, χ = 14.023, P < 0.0001, respectively), ALP (25 mg/kg: 2.35 ± 0.30 ng/ml vs. 3.28 ± 0.20 ng/ml, χ = 4.101, P < 0.0001; 50 mg/kg: 2.34 ± 0.10 ng/ml vs. 3.28 ± 0.20 ng/ml, χ = 2.033, P < 0.0001, respectively), and NO levels (25 mg/kg: 25.92% ± 2.30% vs. 38% ± 2.09%, χ = 17.103, P < 0.0001; 50 mg/kg: 24.74% ± 4.10% vs. 38% ± 2.09%, χ = 25.050, P = 0.001, respectively) compared to morphine group.</p><p><b>Conclusion</b>It seems that genistein administration might improve liver damages induced by morphine in mice.</p>

4.
IJRM-International Journal of Reproductive Biomedicine. 2016; 14 (2): 95-102
in English | IMEMR | ID: emr-178685

ABSTRACT

Background: The predominant phytoestrogen in soy and derived products is the isoflavone Genistein. Genistein has antioxidant properties. Morphine is a main psychoactive chemical in opium that can increase the generation of free radicals and therefore it could adversely affects the spermatogenesis


Objective:The main goal was to investigate whether the Genistein could protect morphine adverse effects on sperm cells viability, count, motility, and testis histology and testosterone hormone and nitric oxide in blood serum


Materials and Methods:In this study, various doses of Genistein [0, 1, 2, and 3 mg/kg] and Genistein plus morphine [0, 1, 2, and 3 mg/kg] were administered interaperitoneally to 48 male mice for 30 consequent days. These mice were randomly assigned to 8 groups [n=6] and sperm parameters [sperm cells viability, count, motility and morphology], testis weight and histology, testosterone hormone [ELISA method], FSH and LH hormones [immunoradiometry] and serum nitric oxide [griess assay] were analyzed and compared


Results: The results indicated that morphine administration significantly decreased testosterone [0.03 ng/mg] LH and FSH level, histological parameters, count, viability [55.3%], morphology and motility of sperm cells [1%], testis weight [0.08 gr] and increase nitric oxide compared to saline group [p=0.00]. However, administration of Genistein and Genistein plus morphine significantly boosted motility, morphology, count, viability of sperm cells, seminiferous tubules diameter, germinal thickness, testosterone, LH and FSH while decrease nitric oxide level in all groups compared to morphine group [p<0.025]


Conclusion:It seems that Genistein administration could increase the quality of spermatozoa and prevent morphine- induced adverse effects on sperm parameters

5.
Clinical and Experimental Reproductive Medicine ; : 193-198, 2016.
Article in English | WPRIM | ID: wpr-54503

ABSTRACT

OBJECTIVE: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect. G6PD plays a key role in the pentose phosphate pathway, which is a major source of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH provides the reducing equivalents for oxidation-reduction reductions involved in protecting against the toxicity of reactive oxygen species such as H₂O₂. We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of H₂O₂, which could potentially affect their motility and viability, resulting in an increased susceptibility to infertility. METHODS: Semen samples were obtained from four males with G6PD deficiency and eight healthy males as a control. In both groups, motile sperms were isolated from the seminal fluid and incubated with 0, 10, 20, 40, 60, 80, and 120 µM concentrations of H2O2. After 1 hour incubation at 37℃, sperms were evaluated for motility and viability. RESULTS: Incubation of sperms with 10 and 20 µM H₂O₂ led to very little decrease in motility and viability, but motility decreased notably in both groups in 40, 60, and 80 µM H₂O₂, and viability decreased in both groups in 40, 60, 80, and 120 µM H₂O₂. However, no statistically significant differences were found between the G6PD-deficient group and controls. CONCLUSION: G6PD deficiency does not increase the susceptibility of sperm to oxidative stress induced by H₂O₂, and the reducing equivalents necessary for protection against H₂O₂ are most likely produced by other pathways. Therefore, G6PD deficiency cannot be considered as major risk factor for male infertility.


Subject(s)
Humans , Male , Glucose-6-Phosphate , Glucosephosphate Dehydrogenase Deficiency , Glucosephosphate Dehydrogenase , Infertility , Infertility, Male , NADP , Oxidation-Reduction , Oxidative Stress , Pentose Phosphate Pathway , Reactive Oxygen Species , Risk Factors , Semen , Spermatozoa
6.
IJPM-International Journal of Preventive Medicine. 2013; 4 (12): 1402-1413
in English | IMEMR | ID: emr-138123

ABSTRACT

Sirtuin1 is an enzyme that deacetylates histones and several non-histone proteins including P53 during the stress. P300 is a member of the histone acetyl transferase family and enzyme that acetylates histones. Hereby, this study describes the potency combination of Salermide as a Sirtuin1 inhibitor and cholera toxin B [CTB] as a P300 activator to induce apoptosis Michigan Cancer Foundation-7 [MCF-7] and MRC-5. Cells were cultured and treated with a combination of Salermide and CTB respectively at concentrations of 80.56 and 85.43 micro mol/L based on inhibitory concentration 50 indexes at different times. The percentage of apoptotic cells were measured by flow cytometry. Real-time polymerase chain reaction was performed to estimate the messenger ribonucleic acid expression of Sirtuin1 and P300 in cells. Enzyme linked immunosorbent assay and Bradford protein techniques were used to detect the endogenous levels of total and acetylated P53 protein generated in both cell lines. Our findings indicated that the combination of two drugs could effectively induced apoptosis in MCF-7 significantly higher than MRC-5. We showed that expression of Sirtuin1 and P300 was dramatically down-regulated with increasing time by the combination of Salermide and CTB treatment in MCF-7, but not MRC-5. The acetylated and total P53 protein levels were increased more in MCF-7 than MRC-5 with incubated combination of drugs at different times. Combination of CTB and Salermide in 72 h through decreasing expression of Sirtuin1 and P300 genes induced acetylation of P53 protein and consequently showed the most apoptosis in MCF-7 cells, but it could be well-tolerated in MRC-5. Therefore, combination of drugs could be used as an anticancer agent


Subject(s)
Humans , Cell Line , Naphthols , Cholera Toxin , MCF-7 Cells
7.
IJFS-International Journal of Fertility and Sterility. 2011; 5 (3): 142-147
in English | IMEMR | ID: emr-144151

ABSTRACT

Sildenafil is a selective inhibitor of cyclic-guanosine monphosphat-specific phosphodiesterase type 5. It increases intracellular nitric oxide [NO] production in some cells. There are reports on its positive effect on uterine circulation, endometrial thickness, and infertility improvement. Endometrial epithelial cells [EEC] play an important role in embryo attachment and implantation. The present work investigates the effect of sildenafil on human EEC and their NO secretion in vitro. In this experimental in vitro study, endometrial biopsies [n=10] were washed in a phosphate buffered solution [PBS] and digested with collagenase I [2 mg/ml in DMEM/F12 medium] at 37°C for 90 minutes. Epithelial glands were collected by sequential filtration through nylon meshes [70 and 40 micro m pores], respectively. Epithelial glands were then treated with trypsin to obtain individual cells. The cells were counted and divided into four groups: control and 1, 10, and 20 micro M sildenafil concentrations. Cells were cultured for 15 days at 37°C and 5% CO[2]; the media were changed every 3 days, and their supernatants were collected for the NO assay. NO was measured by standard Greiss methods. Data were analyzed by one way ANOVA. There was no significant difference between groups in cell count and NO secretion, but the level of NO increased slightly in the experimental groups. The 10 micro M dose showed the highest cell count. EEC morphology changed into long spindle cells in the case groups. Sildenafil [1, 10, and 20 micro M] showed a mild proliferative effect on human EEC numbers, but no significant change was seen in NO production


Subject(s)
Humans , Female , Piperazines/metabolism , Nitric Oxide/metabolism , Endometrium/cytology , Epithelial Cells , Phosphodiesterase Inhibitors
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