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1.
Int J Reprod Biomed ; 21(4): 285-294, 2023 May.
Artigo em Inglês | MEDLINE | ID: mdl-37260555

RESUMO

Background: Cyclophosphamide (CP) has clinical applications in treating diverse malignancies and autoimmune disorders; at the same time, it also has harmful effects on the body tissues, particularly the genitals. The most significant side effects of CP are changing the reproductive system's function and infertility. Objective: This study determines the Ephedra hydroalcoholic extract (EP) role on testicular tissue and the pituitary-gonadal axis in CP-treated male rats. Materials and Methods: In this experimental study, 48 adult Wistar rats were separated into 6 groups (n = 8/each): control, sham, CP recipients, and CP recipients with gavage-fed EP (250, 500, and 1000 mg/kg). On the 29th day, the blood of the weighed animals' was drawn from their heart, and serum concentrations of follicle-stimulating hormone, luteinizing hormone, and testosterone were measured. After preparing testicular tissue segments, cells were counted. Results: While CP decreased follicle-stimulating hormone, luteinizing hormone, and testosterone levels (p < 0.05), the use of EP changed them and even reached the control. Serum gonadotropin-releasing hormone increased significantly in all EP groups compared to the control and CP groups. Compared to the control, a significant decrease in total antioxidant capacity and plasma glutathione peroxidase was observed in the CP groups. EP (all doses) significantly increased their concentration compared to the CP group (p < 0.05); significant reduction in serum total oxidant status and malondialdehyde in CP groups changed by EP (p < 0.05). Although CP's role on spermatogonia counts (57.5 ± 5.2 in CP, 67.1 ± 6.0 in control), higher doses of EP had no significant effect on this but did affect spermatocyte and spermatid cells count. Conclusion: Due to its antioxidant characteristics, EP mitigated the effects of CP on the investigated parameters in rats.

2.
ARYA Atheroscler ; 19(2): 23-29, 2023 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38883567

RESUMO

BACKGROUND: Coronary Artery Diseases (CAD) are the leading cause of Myocardial Infarction (MI). However, their underlying etiology can be found in the interplay between environmental and genetic factors. On the other hand, it has been shown that Extracellular Matrix (ECM) proteins, such as Thrombospondins (TSP), play a crucial regulatory role in vascular pathologies, including atherogenesis. TSPs are extracellular proteins responsible for intercellular and cell-ECM interactions and are involved in regulating functional responses. Recently, a missense mutation in the TSP-4 gene has been reported to potentially increase the risk of CADs. The present study aimed to investigate the role of rs1866389 Guanosine to Cytosine (G/C) Single Nucleotide Polymorphism (SNP) of the TSP-4 gene on the prevalence of premature MI in southern Iran. METHOD: The present case-control study included 100 patients with premature MI and 100 healthy individuals. The DNA extracted from the blood samples of the participants underwent Polymerase Chain Reaction (PCR) for the sequence of the TSP-4 gene. Afterward, the frequency of C (mutated) and G (normal) alleles of the TSP-4 gene was evaluated in the case and control groups. RESULTS: According to our findings, there was no significant intergroup difference in gender, age, and smoking status. However, the case group was significantly higher in the prevalence of Diabetes mellitus (DM), Hyperlipidemia (HLP), and Hypertension (HTN) compared to the control group. Moreover, 22%, 49%, and 29% of the case group had CC, GC, and GG genotypes in the TSP-4 gene, respectively, while the prevalence of CC, GC, and GG genotypes were 10%, 44%, and 46% in the control group. Also, the prevalence of allele C was significantly higher in the case group (47%) compared to the control group (33%, P=0.043), showing its significant association with the increased risk of premature MI (OR = 1.80; 95% CI = 1.01-3.19). CONCLUSIONS: The rs1866389 G/C SNP of the TSP-4 gene significantly increased the risk of premature MI in the population of southern Iran. Thus, such mutated gene can be used as a target for gene therapy or a marker for early detection of individuals at high risk for CADs.

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