ABSTRACT
There is increasing evidence that gender impacts the onset and progression of cardiovascular pathology. However, it is vastly unclear how this variable determines the ultimate outcomes, particularly in the setting of pressure overload-induced left ventricular hypertrophy (LVH). This study was carried out to fill this gap, at least in part, by assessing myocardial expression of G protein-coupled estrogen receptor (GPER) in female and male rats afflicted with LVH. Both female and male rats underwent abdominal aorta banding to induce LVH or were kept intact as control groups. At the end of the experiment, carotid artery catheterization was performed to measure systolic (SBP) and diastolic (DBP) blood pressure. Fibrosis and cardiomyocyte cross-sectional area were assessed by conventional histological analyses. Protein and mRNA expression were evaluated by Western blot/immunofluorescence staining and real-time RT-PCR technique, respectively. In LVH groups, male rats exhibited higher SBP and DBP, heart weight to body weight ratio, and fibrosis compared with female rats. However, both sexes showed a similar increase in cardiomyocyte size after LVH induction. In female, but not in male rats, LVH instigated the GPER mRNA and protein expression in the heart. These results, confirm a significant interaction between gender and myocardial remodeling in terms of GPER expression. Thus, it can be argued that sex differences in the cardiac GPER expression may be responsible for sex differences in the pressure overload-induced LVH. In other words, the female heart seems to unleash stronger protection against pressure overload than that of males in light of a higher GPER expression.
ABSTRACT
OBJECTIVE: Men's sexual health plays an important role in male fertility and childbearing, as it is associated with factors such as sexual desire, healthy spermatogenesis, and erectile function. In various cultures, medicinal plants have been utilized to address male sexual issues, including infertility and erectile dysfunction. Despite recent advancements in medical science for treating male impotence, some men opt for herbal supplements as an alternative, given that numerous herbs have the potential to enhance male sexual performance. The Apiaceae family is one of the oldest plant families used for medicinal purposes. Ferula, a genus within this family, comprises approximately 170 different species worldwide. Members of this genus possess numerous therapeutic properties due to the presence of various compounds. This article aims to explore the potential impacts of Ferula plants on the male reproductive system. METHODS: This review article was prepared by searching for terms including Ferula and "aphrodisiac," Ferula and "spermatogenesis," and Ferula and "male reproductive system." Relevant information was gathered through electronic databases, including ISI Web of Knowledge, PubMed, and Google Scholar. RESULTS: The findings indicated that relatively comprehensive studies have been conducted in this area, revealing that certain Ferula species have been employed in folk medicine to boost fertility and libido. Recent research has corroborated these effects. CONCLUSION: It is hoped that new aphrodisiac compounds with fewer side effects can be isolated from Ferula plants in the future.
ABSTRACT
BACKGROUND: 1, 25-dihydroxy Vitamin D3 (VitD) attenuates left ventricular hypertrophy (LVH), but the mechanisms remain to be portrayed in-depth. The small GTPase Rac1 plays a pivotal role in cardiovascular pathology, especially LVH. Here, we tested whether VitD exerts its anti-LVH effects by counteracting the small GTPase Rac1 expression. METHODS: In Wistar rats, pressure overload-induced LVH was created by abdominal aortic banding. The animals were intraperitoneally administered VitD (0.1 µg/kg/d). Blood pressure was measured via carotid artery cannulation. Real-time RT-PCR and Western blotting were performed to assess the mRNA and protein expression, respectively. Myocardium was stained for determination of cardiomyocytes area and fibrosis. Lipid peroxidation levels and the activities of antioxidant enzymes were measured in left ventricular tissue. RESULTS: VitD significantly reduced hypertrophy markers (blood pressure, heart-to-body weight ratio, cardiomyocytes area, fibrosis as well as atrial and brain natriuretic peptides mRNA levels) compared to untreated groups (P < 0.05). VitD also improved the activity of antioxidant enzymes and reduced lipid peroxidation levels in the myocardium (P < 0.05). LVH hearts of untreated animals displayed a significant increase in Rac1 expression compared with the control group (P < 0.05). In contrast, cardiac Rac1, at either mRNAs or protein levels, was markedly lower in LVH animals receiving VitD compared with their untreated counterparts (P < 0.05). CONCLUSION: Our findings attest that VitD mitigates hallmarks of LVH imparted by pressure overload. Notably, VitD appears to perform its anti-LVH function partly through small GTPase Rac1 suppression. This, in turn, provides a robust incentive to consider VitD before LVH culminates in HF devastating disease.
