Bee Bread Ameliorates Vascular Inflammation and Impaired Vasorelaxation in Obesity-Induced Vascular Damage Rat Model: The Role of eNOS/NO/cGMP-Signaling Pathway.

Obesity and hyperlipidemia are major risk factors for developing vascular diseases. Bee bread (BB) has been reported to exhibit some biological actions, including anti-obesity and anti-hyperlipidemic. This study aims to investigate whether bee bread can ameliorate vascular inflammation and impaired vasorelaxation activity through eNOS/NO/cGMP pathway in obese rats. Forty male Sprague-Dawley rats were randomly divided into four groups (n = 10/group), namely: control (normal group), obese rats (OB group), obese rats treated with bee bread (0.5 g/kg/day, OB/BB group) and obese rats treated with orlistat (10 mg/kg/day, OB/OR group). The latter three groups were given a high-fat diet (HFD) for 6 weeks to induced obesity before being administered with their respective treatments for another 6 weeks. After 12 weeks of the total experimental period, rats in the OB group demonstrated significantly higher Lee obesity index, lipid profile (total cholesterol, triglyceride, low-density lipoprotein), aortic proinflammatory markers (tumor necrosis factor-α, nuclear factor-κß), aortic structural damage and impairment in vasorelaxation response to acetylcholine (ACh). Bee bread significantly ameliorated the obesity-induced vascular damage manifested by improvements in the lipid profile, aortic inflammatory markers, and the impaired vasorelaxation activity by significantly enhancing nitric oxide release, promoting endothelial nitric oxide synthase (eNOS) and cyclic guanosine monophosphate (cGMP) immunoexpression. These findings suggest that the administration of bee bread ameliorates the impaired vasorelaxation response to ACh by improving eNOS/NO/cGMP-signaling pathway in obese rats, suggesting its vascular therapeutic role.

Histological changes of female reproductive organs subjected to different jumping exercise intensities and honey supplementation in rats.

BACKGROUND: We assessed histopathological changes of ovaries and uterus in female rats subjected to different jumping exercise intensities combined with honey supplementation at one g/kg body weight/day. METHODS: A total of 72 rats were divided into six groups, 12 rats in each: control (C), 20 and 80 jumps (20E, 80E), honey (H), and 20 and 80 jump with honey (20EH, 80EH). RESULTS: The endometrium was significantly thicker in the rats in H, 20EH and 80EH groups compared to C, 20E, and 80E. The myometrium thickness was significantly lower in 80E and significantly higher in 80EH compared to C, respectively. There was significantly higher myometrium thickness in 20EH and 80EH compared to 20E and 80E and H. The number of glands of the uterus in 20E and 80E was significantly lower than C. However, there was a significantly higher number of glands in H, 20EH, and 80EH compared to 20E and 80E. The numbers of uterus vessels were significantly lower in 80E compared to 20E. However, the numbers of vessels were significantly higher in H, 20EH, and 80EH compared to 80E. The number of ovarian haemorregia was significantly lower in 20E, 80E, H, 20EH, and 80EH compared to C. The number of corpora lutea was significantly lower in 80EH, H, 80E, and 20E compared to C. However, the number of corpora lutea was significantly higher in 20EH compared to J20 and H. CONCLUSION: This study suggested that jumping exercises in particularly high-intensity exercise may induce histopathological changes in uterus and ovary in rats, and honey supplementation may ameliorate these effects.

Raised leptin concentrations in feto-placental tissues from women with preeclampsia.

OBJECTIVE: The aim of this study was to estimate the levels of leptin in the amnion, chorion laeve, and placenta and to examine for any differences in leptin levels in these tissues from preeclamptic and normotensive pregnant women. METHOD: Fresh samples of amnion, chorion laeve, and placenta were obtained from 10 normotensive and 10 preeclamptic women following vaginal delivery. After repeated washing with Krebs Heinsleit solution, 2 g of each tissue were homogenized separately. Following centrifugation, the supernatant was removed and stored at -80 degrees C for analysis of leptin at a later date. Leptin in supernatants from homogenates was measured using commercially available radioimmunoassay (RIA) Kits. Statistical analysis was performed using student's t-test for independent samples and all results are expressed as mean +/- SEM. RESULTS: Leptin concentrations were significantly higher in all the three tissues from preeclamptic women when compared to the corresponding tissues from normotensive controls (0.52 +/- 0.1 vs. 1.15 +/- 0.41; 0.99 +/- 0.16 vs. 2.19 +/- 0.71; and 10.28 +/- 1.06 vs. 13.95 +/- 1.13 in the amnion, chorion laeve, and placenta, respectively, from normotensive pregnant women and women with preeclampsia; p < 0.05). CONCLUSION: Leptin concentration is significantly raised in fetoplacental tissues from women with preeclampsia. Its role in preeclampsia remains unclear and it is not possible to say from this study if the raised levels of leptin evident in placentas from preeclamptic women are a cause or consequence of preeclampsia, although the latter seems more likely.