6 research outputs found
Evaluation of combined therapeutic effects of hydrogen sulfide donor sodium hydrogen sulfide and phosphodiesterase type-5 inhibitor tadalafil on erectile dysfunction in a partially bladder outlet obstructed rat model
Aims: To evaluate the impacts of hydrogen sulfide (H2S) donor, sodium hydrogen sulfide (NaHS), and phosphodiesterase type-5 inhibitor (PDE5i), tadalafil per se and their combination treatment on partial bladder outlet obstruction (PBOO)-induced erectile dysfunction (ED). Methods: Sprague-Dawley rats were equally divided into five groups: (a) sham-operated control; (b) PBOO; (c) PBOO-treated with NaHS (5.6 mg/kg/day, ip); (d) PBOO-treated with tadalafil (2 mg/kg/day, oral); and (e) PBOO-treated with combination of NaHS and tadalafil. The obstruction was created by urethral ligation for 6 weeks. In vivo erectile responses, in vitro relaxant and contractile responses in penile tissue as well as protein expression of nitric oxide synthases (NOS), H2S synthesis enzymes, oxidative stress, hypoxia, fibrosis markers, and the smooth muscle/collagen ratio and apoptosis were analyzed. Results: Combined treatment entirely returned increased bladder mass, reduced erectile responses, relaxation responses to acetylcholine, and electrical field stimulation in obstructed rats, while partial amelioration was observed after mono-treatment. Decreased neuronal NOS and 3-mercaptopiruvate transferase enzyme expressions in penile tissue from obstructed rats were also entirely restored by the combined treatment. Mono-treatment partially improved increased hypoxia, oxidative stress, fibrosis markers, decreased smooth muscle mass, and H2S levels, while combined therapy completely recovered. Conclusions: The combination therapy with H2S donor and PDE5i had positive effects on erectile responses through the improvement of ischemia-induced morphological and functional penile alterations in obstruction. H2S and NO may likely play a synergistic role in the regulation of erectile function and have constructive effects on clinical outcomes in male patients with ED and benign prostatic hyperplasia/lower urinary tract symptoms
The beneficial effect of clove essential oil and its major component, eugenol, on erectile function in diabetic rats.
Diabetic men are at a higher risk of erectile dysfunction (ED). A tropical plant, clove (Syn. Eugenia caryophyllata, Caryophyllus aromaticus L., Syzygium aromaticum (L.) Merr. & L.M. Perry) from the Myrtaceae family has displayed aphrodisiac activity. The present research aimed to investigate the impacts of clove essential oil (CEO) and the ingredient of CEO, eugenol (E) on ED in diabetic rats. We divided Sprague-Dawley rats into control and diabetic groups. Erectile function was evaluated before and after CEO and E intracavernosal injection. CEO- and E-induced relaxation responses were investigated in isolated corpus cavernosum (CC) using various inhibitors. The intracavernous administration of CEO and E restored erectile responses in diabetic rats. CEO and E induced remarkable relaxation in all groups. CEO- and E-induced relaxation responses were partially inhibited after pre-contraction with KCl. Tetraethylammonium and glibenclamide inhibited the relaxation response to CEO. Glibenclamide inhibited maximum relaxation to E. The inhibitors of nitric oxide synthase (NOS), soluble guanylyl cyclase and nifedipine did not change CEO- and E-induced relaxation responses. The current results suggest that CEO and the major compound of the essential oil, E improved diabetes-induced ED in rats, and CEO caused CC relaxation via K channels independently NO signalling pathway
The beneficial effect of clove essential oil and its major component, eugenol, on erectile function in diabetic rats.
Diabetic men are at a higher risk of erectile dysfunction (ED). A tropical plant, clove (Syn. Eugenia caryophyllata, Caryophyllus aromaticus L., Syzygium aromaticum (L.) Merr. & L.M. Perry) from the Myrtaceae family has displayed aphrodisiac activity. The present research aimed to investigate the impacts of clove essential oil (CEO) and the ingredient of CEO, eugenol (E) on ED in diabetic rats. We divided Sprague-Dawley rats into control and diabetic groups. Erectile function was evaluated before and after CEO and E intracavernosal injection. CEO- and E-induced relaxation responses were investigated in isolated corpus cavernosum (CC) using various inhibitors. The intracavernous administration of CEO and E restored erectile responses in diabetic rats. CEO and E induced remarkable relaxation in all groups. CEO- and E-induced relaxation responses were partially inhibited after pre-contraction with KCl. Tetraethylammonium and glibenclamide inhibited the relaxation response to CEO. Glibenclamide inhibited maximum relaxation to E. The inhibitors of nitric oxide synthase (NOS), soluble guanylyl cyclase and nifedipine did not change CEO- and E-induced relaxation responses. The current results suggest that CEO and the major compound of the essential oil, E improved diabetes-induced ED in rats, and CEO caused CC relaxation via K channels independently NO signalling pathway
The beneficial effect of clove essential oil and its major component, eugenol, on erectile function in diabetic rats
Diabetic men are at a higher risk of erectile dysfunction (ED). A
tropical plant, clove (Syn. Eugenia caryophyllata, Caryophyllus
aromaticus L., Syzygium aromaticum (L.) Merr. \& L.M. Perry) from the
Myrtaceae family has displayed aphrodisiac activity. The present
research aimed to investigate the impacts of clove essential oil (CEO)
and the ingredient of CEO, eugenol (E) on ED in diabetic rats. We
divided Sprague-Dawley rats into control and diabetic groups. Erectile
function was evaluated before and after CEO and E intracavernosal
injection. CEO- and E-induced relaxation responses were investigated in
isolated corpus cavernosum (CC) using various inhibitors. The
intracavernous administration of CEO and E restored erectile responses
in diabetic rats. CEO and E induced remarkable relaxation in all groups.
CEO- and E-induced relaxation responses were partially inhibited after
pre-contraction with KCl. Tetraethylammonium and glibenclamide inhibited
the relaxation response to CEO. Glibenclamide inhibited maximum
relaxation to E. The inhibitors of nitric oxide synthase (NOS), soluble
guanylyl cyclase and nifedipine did not change CEO- and E-induced
relaxation responses. The current results suggest that CEO and the major
compound of the essential oil, E improved diabetes-induced ED in rats,
and CEO caused CC relaxation via K+ channels independently NO signalling
pathway
Palladium Metal Nanocomposites Based on PEI-Functionalized Nitrogen-Doped Graphene Quantum Dots: Synthesis, Characterization, Density Functional Theory Modeling, and Cell Cycle Arrest Effects on Human Ovarian Cancer Cells
In this study, the synthesis, characterization, density
functional
theory calculations (DFT), and effect of polyethylenimine (PEI)-functionalized
nitrogen-doped graphene quantum dots (PEI N-GQDs) and their palladium
metal nanoparticles nanocomposites (PdNPs/PEI N-GQDs) on cancer cells
were extensively investigated. The focus also includes investigating
their cytotoxic and apoptotic effects on ovarian cancer cells, which
pose a serious risk to women’s health and have high death rates
from delayed diagnosis, inadequate response to treatment, and decreased
survival. Graphene quantum dots and their palladium nanocomposites
were differentially effective against ovarian cancer cell lines. In
particular, the smaller particle size and morphology of PdNPs/PEI
N-GQDs nanocomposites compared with PEI N-GQDs probably enhance their
activity through highly improved uptake by cells. These findings emphasize
the importance of particle size in composite drugs for efficient cancer
treatment. DFT results revealed that the Pd-containing nanocomposite,
with a smaller highest occupied molecular orbital–lowest unoccupied
molecular orbital gap, exhibited higher reactivity and anticancer
effects in human ovarian cancer cell line, OVCAR-3. Significantly,
the application of nanocomposites to ovarian cancer cells initiated
apoptosis, offering valuable insights into the intricate interplay
between nanomaterials and cancer biology