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Background: To investigate bromocriptine's therapeutic benefits alongside clomiphene citrate in the induction of ovulation in polycystic ovary syndrome patients with infertility. No significant difference was found between the two groups, according to the success rate of ovulation induction in the control group and observation group. No significant differences were found between two groups on the day of hCG in the blood tests, E2, and P were found between the two groups, but LH was higher, and PRL and T were significantly lower in the observation group than those in the control group. No significant differences in the levels of E2 and P were found in the observation group relative to that in the control group, and the endometrial thickness in the observation group was significantly higher than that in the control group on day 7 after hCG injection. Conclusions: BCT alone, as with CC alone, can raise the success rate of ovulation induction-assisted pregnancy in PCOS patients, reduce the incidence of PRL, LH, and T, and T, as well as raise the endometrial thickness in the implantation window. According to those results, dopamine agonist BCT can reduce pituitary hormone and androgen levels, reduce endometrial vascular resistance, and increase endometrial blood supply to improve PCOS patients with infertility.
Source link: https://doi.org/10.4103/2096-2924.224917
Insulin and triglycerides were found in the basal plasma of ID horses, as well as lower adiponectin levels in comparison to non-ID horses. Compared to non-ID horses, ID horses had slower glucose clearance rates, which resulted in a longer stay in the positive phase and higher insulin levels at 75 min. In non-ID versus ID horses, the feeding challenge was slower. In all horses, Bromocriptine therapy decreased plasma prolactin and cholesterol, as well as elevated adiponectin concentrations. In addition, bromocriptine decreased glucose clearance rates in both groups of horses, increased time in the positive phase of the CGIT, and raised insulin levels at 75 min. The postprandial glycemic and insulin response following the oats meal was lower after bromocriptine therapy in all horses. These results show that EA's physiological responses in horses may be different than those of other animals.
Source link: https://doi.org/10.3389/fvets.2022.889888
There are no data available on data assessing the presence of CRP in hyperprolactinemic syndrome and the effect of bromocriptine on CRP concentration. Hence, the current study was intended to determine the concentration of CRP in a variety of women with hyperprolactinemic amenorrhea as well as the effects of bromocriptine on CRP concentrations. The control group's mean CRP concentration was 1. 38 mg/L, which is statistically lower than the average CRP concentration of 6. 35 mg/L of the patients before bromocripine therapy. respectively, the relationship between serum prolactin level and serum CRP level before and after bromocriptine therapy was not statistically significant: r= 0. 24, P > 0. 05, and r = 0. 12, P > 0. 2, respectively. The present report revealed that women with hyperprolactinemic amenorrhea are strongly associated with elevated CRP and bromocriptine therapy significantly reduced CRP, indicating a potential anti-inflammatory agent in addition to prolactin's lowering effects.
Source link: https://doi.org/10.33762/mjbu.2008.48346
In order to determine the effect of injection of bromocriptine on the early stages of pregnancy, ten males were used for mating, and this was discovered by measuring the weights of some component of female reproduction. These findings also demonstrated the effectiveness of bromocriptine in reducing the production of prolactin hormones and the onset of its negative influence on mice's early stages of pregnancy by its effects on the ovaries and uterus.
We performed a high throughput assay with a chemical library containing a total of 3280 bioactive smallmolecules to determine the novel inhibitors of endoplasmic reticulum-induced cell death. Cyclosporine A and bromocriptine were both identified as potent inhibitors of thapsigargiin-induced cell death. Theinhibition effect of cyclosporine A and bromocriptine was limited to only thapsigargin-mediated cell death, according to the inhibition. We propose that the induction of a protective unfolded protein response by thesecompounds provides resistance to cell death. In summary, we identified compounds that may have triggered cell deathmechanisms triggered by ER stress.
Flatworm G protein coupled receptors' diversity and uniqueness allows for the identification of ligands useful in investigating flatworm disease research or as therapeutics for treating parasitic flatworm infections. Flatworm GPCR screening methods must be used to support this discovery process. To speed up this process, technologies suitable for mammalian GPCR high throughput screening should be used. We demonstrate the use of a genetically coded cAMP biosensor for determining the properties of an abundantly distributed planarian serotonergic GPCR.
Source link: https://doi.org/10.1016/j.ijpddr.2016.06.002
Bromocriptine was firmly bound to NF-u03baB pathway proteins as shown by molecular docking and interacted more closely with DNA-bound NF-u03baB-u03baB than free NF-u03baB, indicating that bromocriptine may reduce NF-u03baB attachment to DNA than free NF-u03baB, indicating that bromocriptine inhibits NF-u03baB NF-u03baB-u03baBaB pathway proteins in NF-u03baBaBaB-u03baB NF-u03baBaB NF-u03baBaB-u03baB-u03baB'u03baBaB-u03baB binding to DNA. In addition, bromocriptine reduced NF-u03baB production by a SEAP-driven NF-u03baB reporter cell assay, according to a SEAP-driven NF-u03baB reporter cell assay. In a panel of 60 NCI cell lines, the expression of MDR-conferring ABC-transporters and other resistance-mediating variables did not correspond to cellular response to bromocriptine. There was no correlation between cell response to bromocriptine and anticancer drugs commonly used in MDR. Our findings show that bromocriptine inhibited drug-resistant tumor cells with different resistance mechanisms in a hormone-independence manner. Bromocriptine may be used for repurposing in cancer therapy as refractory and otherwise drug-resistant tumors pose a significant obstacle to successful cancer chemotherapy.
Source link: https://doi.org/10.3389/fphar.2018.01030
Methods: The thin film technique allowed curcumin and BR liposome preparations to be carried out, and the amounts of purified drug and its release were analyzed. The human lung cancer cells were exposed to BR and curcumin liposomes for 12, 24, and 48 h after dose determination, respectively, demonstrating the sensitivity and apoptosis assays. In this study, in vitro anti-cancer effects of former nano-formulations on lung cancer cells were confirmed, but no cytotoxicity effects of these nano-preparations were observed in the normal cells.
Patients with brain injury are affected by central hyperthermia. It is also associated with adverse outcomes in the brain injury patient. A 34-year-old male with a right thalamic hemorrhage extending to the midbrain and into the ventricles. The infectious workup was unremarkable. Bromocriptine was introduced, resulting in central hyperthermia control. In conclusion, there was no conclusion. Diagnosing and regulating central hyperthermia can be difficult. As we have shown, bromocriptine can be helpful.
Source link: https://doi.org/10.1155/2017/1712083
The dopamine D2 receptor agonist bromocriptine has been used extensively to treat human breast tumor and prolactinoma by reduction of hyperprolactinemia and tumor cell apoptosis, respectively, but the precise mechanism of bromocriptine induction of pituitary tumor apoptosis remains unclear. Currently, caveolin-1 is thought to be a negative regulator of cell proliferation and a promoter of apoptosis by blocking signal transduction between cell surface membrane receptors and intracellular signaling protein cascades. Hence, the GH3 cell line is a good starting point for investigating bromocriptine's molecular action on prolactinoma. After bromocriptine treatment, phosphorylation of caveolin-1 in tyrosine 14 was boosted, suggesting that bromocriptine-induced phosphorylation of caveolin-1 may contribute to sensitivity to apoptosis in GH3 cells exposed to bromocriptine. Conclusion Our results show that caveolin-1 enhances the risk of apoptosis induction in pituitary adenoma GH3 cells and may contribute to tumor shrinkage after medical bromocriptine therapy.
Source link: https://doi.org/10.1186/1475-2867-7-1
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