Protective role of curcumin against 2,3,7,8-tetrachlorodibenzo-dioxin-induced histological and biochemical changes in fundic mucosa of the adult rat stomach

2,3,7,8-Tetrachlorodibenzo-dioxin [TCDD] is released into the environment from different activities and industrial sources, with a higher incidence of gastric exposure. This work aimed to study the histological and biochemical changes induced by TCDD in the fundic mucosa and the possible protective role of curcumin against these changes. Thirty adult female albino rats were classified into three groups: the control group [group I]; the TCDD group [group II], in which rats received 100 microg/kg TCDD orally for 3 months; and the curcumin+TCDD group [group III], in which rats received an oral dose of 80 mg/kg curcumin in concurrence with TCDD for 3 months. The serum level of the gastrin hormone was measured. Samples from the fundus of the stomach were stained with H and E, Van Gieson, and PAS/alcian blue and for immunohistochemical detection of aryl hydrocarbon receptors [AHR] and chromogranin A. Morphometric and electron microscopic studies were also carried out. Hyperplasia and metaplastic mucosal changes, together with enteroendocrine cell hyperplasia, were evident. Moreover, glandular degeneration, areas of atrophic gastritis, cellular apoptosis, and gastric ulcers were detected. The previous results could be explained by both TCDD-induced hypergastrinemia and increased AHR expression. In contrast, curcumin appeared to have a propitious protective effect against TCDD-induced gastric affection. Most of the TCDD-induced gastric changes were not observed in group III. It was concluded that the gastric mucosa is sensitive to the toxic effects of TCDD and curcumin can be used to avoid TCDD-induced gastric complications

green tea have an ameliorative effect against cabergoline-induced cardiotoxicity in adult male albino rats? A histological and biochemical study

Cabergoline is an ergot alkaloid derivative with dopamine agonist activity. The use of cabergoline was associated with significantly increased frequency of heart disease. Green tea has been found to prevent many cardiovascular diseases. To determine whether green tea could have an ameliorative effect against myocardial and valvular injury induced by cabergoline toxicity in rats or not. Thirty-six adult albino rats were used in this study. Medications were administered 6 days/week for 3 months by an oral gavage. The animals were divided into three groups; group 1 served as a control. Group II was given 0.5mg/kg cabergoline dissolved in corn oil. In group III, the rats received green tea 1000mg/kg, dissolved in 3ml distilled water along with cabergoline. Venous blood samples were collected. Cardiac enzymes including serum cardiac troponin I, lactate dehydrogenase, and creatine kinase-MB were estimated. All rats were sacrificed and their hearts were dissected out and processed for light and election microscopic examination. Cabergoline administration caused significant increases in the studied cardiac enzymes compared with the control groups. Histologically, evident myocardial lesions were revealed in group II in the form of widely separated and split muscle fibers. Ultrastructurally, the sarcoplasm contained irregular nuclei and bizarre-shaped mitochondria of different sizes. Localized areas of edema, corrugated sarcolemma, and interstitial collagen fibers were observed particularly in areas of myocardial damage. Alterations in the intercalated disc were also revealed. The mitral valve leaflets showed shortening and thickening of their leaflets. Coadministration of green tea with cabergoline caused a significant decrease in the mean troponin-I serum level compared with the cabergoline-treated group, whereas lactate dehydrogenase and creatine kinase -MB levels did not show any significant changes. Structurally, improvements in most myocardial and mitral lesions in the treated group were detected, except for some bizarre-shped mitochondria and interruption of the intercalated discs. Cabergoline has a deleterious effect on the histological structure of cardiac muscle and valves. Green tea could ameliorate some of these effects

Impact of urinary growth hormone/insulin growth factor-i on the development of nephropathy in early-onset and long-term diabetic children

Growth hormone [GH], insulin-like growth factor-I [IGF-I], IGF-binding protein [GH/IGF/IGFBP] axis has been suggested both to maintain normal renal function and to play an important role in the development of diabetic nephropathy [DN], in patients with type 1 diabetes [T1D]. Nephromegaly [NM] and microalbuminuria [MA] are early markers of DN. Study the role of urinary concentrations of GH and IGF-I in the development of DN, in children and adolescents suffering T1D, A total of 50 children and adolescents with T1D of 6-14 years old were recruited from the Pediatric Diabetes Clinic at King Abdulaziz University Hospital, 23 were males and 27 were females. Subjects were divided into two groups; 20 with early-onset diabetes and 30 with long-term diabetes. Both groups were subjected to history-taking, clinical examination including body mass index [BMI], pubertal staging according to the rating of Tanner[1], assessment of glycemic control, measurement of kidney volume [KV], as a marker of glomerular hypertrophy, by ultrasonography [U/S]. The overall rate of MA and NM accounted for 20% [10/50] and 26% [13/50], respectively, being more detected in long-term diabetics than that in patients with early-onset diabetes, with significant difference. Long-term diabetics had significantly higher albumin excretion rate [AER] and urinary GH and IGF-I concentrations than that in early-onset diabetics. The mean BMI, pubertal duration, urinary GH and urinary IGF-I were significantly higher among diabetics positive for MA than that among diabetics negative for MA. our data, which reflect increased mean urinary GH / IGF-I production, strengthen the evidence of an association between GH and MA and NM and also implicate urinary GH/ IGF-I in DN, particularly in children and adolescents with long-term diabetes, increased pubertal duration and poor glycemic contro