Pre-eclampsia (PE) accompanying acute liver and kidney injury has remained a master cause of both fetal and maternal mortality and morbidity. Vasoactive mediators, oxidative stress and inflammatory imbalanceshave an important role in PE pathogenesis. Apelin is an adipokine that improves endothelial dysfunction; has anti-inflammatory and antioxidant effects; moreover, its level reduced during PE. This study aimed to explore the effects of apelin-13 administration on preeclampsia-associated renal dysfunction and proteinuria. Thirty-three pregnant female rats were divided into three groups; group: 1 (normal pregnant rats), group: 2 (preeclamptic rats); where rats were injected subcutaneously with 75 mg L-NAME/ kg body weight/day beginning from 9th to 20th day of pregnancy andgroup 3 (apelin-13 treated preeclamptic rats); In which L-NAME-induced preeclamptic rats were subcutaneously injected with 6 × 10−8 mol apelin-13/kg body weight/twice daily starting from 6th to 20th day of pregnancy. In all groups, mean arterial blood pressure, total urine protein, serum urea, creatinine, nitric oxide (NO), endothelin-1 (ET-1), interleukin–6 (IL-6) and malondialdhyde (MDA) were measured. Histopathological examination of kidney tissues was also done. preeclamptic rats showed significantly increased mean arterial blood pressure, total urine proteins, serum urea, creatinine, ET-1, IL-6, and MDA, but revealed a significantly decreased serum NO level. On the other hand, apelin treatment significantly improved these parameters together with amelioration of kidney histoarchitecture in the treated group. In conclusion, apelin may be a potentially curative candidate for prohibiting kidney damage and have a therapeutic benefit in PE rat models.

Preeclampsia (PE) is one of the commonest causes for maternal and fetal morbidity and mortality. Imbalances of angiogenic factors, oxidative stress, and inflammatory response have a role in the pathogenesis of PE. Data regarding the circulating apelin level and its role in PE remains controversial. This study was formulated to assess the serum apelin level in PE, investigate its correlation with some inflammatory, oxidative stress, and angiogenic proteins in a nitric oxide synthase inhibitor; the N (gamma)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE and determine whether apelin administration could protect against development of PE. 40 healthy adult female albino rats and 10 adult male albino rats were used in this study. The pregnant female rats were randomly divided into three groups: group 1 (normal pregnant group), group 2 (PE-induced group), injected subcutaneously with 75 mg L-NAME/kg bodyweight/day starting from day 9 to 20 of gestation, and group 3 (PE-induced group supplemented with apelin (PE + apelin)); PE induced as before and simultaneously subcutaneously injected with apelin-13 (6 × 10−8 mol/kg bodyweight/twice daily) beginning from day 6 to 20 of gestation. In all groups, blood pressure and urine protein were determined at gestation days (GD) 0, 10, and 18. Moreover, serum apelin, placental growth factor (PLGF), vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), interferon-gamma (IFN-γ), and interleukin-10 (IL-10) levels and serum superoxide dismutase enzyme (SOD) and catalase (CAT) activities of all groups were estimated at the end of experiment. Placental histopathological examination was also performed. PE-induced rats showed significantly decreased serum apelin levels. Moreover, they showed significantly increased blood pressures, urine proteins, sFlt-1, sEng, and IFN-γ (mean arterial blood pressure, urine proteins, sFlt-1, sEng, and IFN-γ showed significant negative correlations with serum apelin level), but it showed significantly decreased VEGF, PLGF, IL-10, SOD, and CAT (VEGF, PLGF, IL-10, and SOD showed significant positive correlations with serum apelin level). In contrast, exogenous apelin administration significantly ameliorated these parameters together with improvement in the placental histoarchitecture in the apelin-supplemented PE group. This study demonstrated the protective effects of apelin administration on the pathogenesis of PE.

Background: Gestational Diabetes Mellitus (GDM) is the most common metabolic disorder that increases the prenatal morbidity. Data regarding the association between circulating chemerin level and GDM remains controversial. On the other hand, Vitamin D deficiency is common in pregnancy and may increase the frequency of GDM. Aim of Study:This study was conducted to examine the effects of Vitamin D 3 supplementation on serum chemerin level and some metabolic parameters in GDM rat model. Material and Methods:Healthy female white albino rats were divided randomly into three groups (n=10 rats): Group I (normal pregnant group); fed on normal diet for five weeks before induction of pregnancy. Group II (GDM-induced); fed High Fat-Sucrose Diet (HFSD) for five weeks before induction of pregnancy then injected Intraperitoneally (I.P) by Streptozotocin (STZ) (25mg/kg) on the 7 th day of gestation. Group III (GDM-induced group supplemented with Vitamin D 3 ); GDM-induced as before and injected Intramuscularly (I. M) with 20,000IU/kg of cholecalciferol on days 1 and 14 of gestation. On the 19 th day of gestation, serum chemerin, estradiol, progesterone, glucose, insulin and Insulin Resistance index (HOMA-IR), Total Cholesterol (TC), Triglycerides (TG), Low Density Lipoprotein-cholesterol (LDL-c), High Density Lipoprotein-cholesterol (HDL-c), Very Low Density Lipoprotein-cholesterol (VLDL-c), Tumor Necrosis Factor alpha (TNF a) and Malondialdehyde (MDA) levels and Serum Superoxide Dismutase (SOD) activity were estimated for all groups.Results: GDM-induced rats showed significantly increased serum glucose, HOMA-IR, TG, TC, LDL-c, VLDL-c, MDA, and TNF a levels while showed significantly decreased serum insulin and HDL-c levels and SOD activity when compared to normal pregnant control rats. GDM-induced rats also showed significantly increased serum chemerin levels that showed significant positive correlations with serum glucose, insulin, HOMA-IR, TG, TC, LDL-c, VLDL-c, MDA, and TNF a levels but showed significant negative correlations with serum HDL-c level and SOD activity. Noteworthy,

Background: Hypertensive disorders of pregnancy, gestational hypertension, and preeclampsia (PE) are exceptionally challenging, as their pathologies and therapeutic management simultaneously influence the mother and embryo, sometimes putting their well-beings at odds with each other. Dysregulated lipid and glucose metabolism may be related to some cases of preeclampsia. Fluctuations in serum apelin levels may be attributed to changes in the serum levels of multiple interrelated factors such as insulin, insulin resistance, inflammatory cytokines, and nephritic damage. Previous studies demonstrated that apelin is an endogenous active peptide with vasodilatory and antioxidative-stress capabilities. Objective: We investigated the relationships among hepatic, nephrotic, and metabolic injuries in different preeclampsia-like mouse models and the potential effect of exogenous apelin administration on hepatic and nephrotic injuries and metabolic disorders in an N-nitro-L-arginine methyl ester (L-NAME) preeclampsia-like Sprague Dawley (SD) rat model. Materials and methods: Forty-three adult female and ten adult male SD rats were involved in this study. The male rats were used to induce pregnancy. The female rats were randomly divided into four equal groups: a non-pregnant group, a normal pregnant group, a group treated with L-NAME to induce preeclampsia, and a group treated with L-NAME and apelin. In all the groups, maternal blood was collected on the 21st day of gestation, and serum samples were used for the determination of systolic blood pressure; the serum uric acid, creatinine, nitric oxide (NO), xanthine oxidase, myeloperoxidase, insulin, glucose, cholesterol, triglyceride (TG), aspartate aminotransferase (AST) and alanine aspartate aminotransferase (ALT) levels; and the HOMA-insulin resistance (HOMA-IR). Results: In rats with pre-eclampsia, the systolic blood pressure; the concentrations of serum uric acid, creatinine, nitric oxide (NO), xanthine oxidase, myeloperoxidase, blood glucose, serum cholesterol, triglycerides, AST, and ALT; and the calculated HOMA-IR were significantly increased compared to those in the rats in the other groups. Additionally, apelin treatment significantly improved these parameters in the apelin-treated group. Conclusion: This study examined the potential mechanisms whereby apelin may act as a curative candidate to reduce hepatic injury and inhibit kidney damage and the development of metabolic disorders in an experimental model of preeclampsia.

Background: Oxidative stress is increased in diabetes mellitus (DM). Ghrelin is a peptide hormone produced by different tissues and its circulating level is decreased in type 1 DM. Recently, it has been shown to have antioxidant properties. Objective: This study was designed to investigate the effects of diabetes mellitus on pituitary testicular functions and the role of ghrelin in the modulation of these effects in a rat model of type 1 diabetes mellitus induced by streptozotocin. Materials and methods: 32 healthy adult male albino rats of initial body weight 170-195 gm were included. Rats were randomly and equally divided into 4 groups, group (1a): Vehicle treated (control) group, group (1b): Ghrelin treated normal group, group (IIa): STZ-diabetic group and group (IIb): Ghrelin treated diabetic group. Rats were weighed and examined for the serum levels of glucose, insulin, FSH, LH& testosterone levels, epididymal sperm count and motility, testicular malondialdhyde (MDA) level and superoxide dismutase (SOD), catalase (CAT) & glutathione peroxidase (GP X ) activities and testicular weight(wt) & histopathology. Results: STZ-induced diabetes significantly decreased the body wt, testes wt, serum insulin, FSH, LH & testosterone levels, epididymal sperm count & motility and testicular SOD, CAT & GP X activities but significantly increased serum glucose & testicular malondialdhyde levels together with deterioration of the testicular histoarchitecture. Moreover, it was found that exogenous administration of ghrelin resulted in a significant recovery of all the above mentioned parameters in the diabetic group, while in the normal group, it was only associated with potentiation of the testicular antioxidant system as well as a significant increase in both the body and testes weights. Conclusion: Ghrelin has a potential protective role against diabetes-induced pituitary testicular dysfunction which may be due to its antioxidant properties and maintenance of glucose & insulin homeostasis.