وائل محمد لطغى- محمد فتحى أبوالنور- طوسون مرسى- شريغ رمضان عبدالغنى- أسماء البكرى- ابراهيم شلش
المؤلفون بالإنجليزي
Wael Mohamed Lotfy; Mohamed Fathy Abouel-Nour; Tosson A. Morsy; Sherif R. AbdelGhany; Asmaa El-Bakri; Ibrahim Shalash
الملخص الانجليزي
Type 1 diabetes (T1D) is initiated by a selective destruction of the insulin-producing β cells found in pancreatic islets of Langerhans by auto antigen-specific inflammatory T cells. Experimental studies suggest that S. mansoni can protect against auto-immune diseases such as TD1. This study aimed at gaining a better understanding of the interaction between S. mansoni infection and chemically induced T1D in mice. A total of 40 female Swiss albino mice were used in all experiments. Animals were divided into 4 groups each of 10 mice. The 1st group was infested with Schistosoma mansoni cercariae and received 130 mg/kg body weight of streptozotocin (STZ) in citrate buffer intraperitoneally. The 2nd group was infected with S. mansoni cercariae, and received citrate buffer intraperitoneally. The 3rd group was received STZ. The 4th
group was injected intraperitoneally with citrate buffer. For all groups the following tests were carried out: determination of the fasting blood glucose level, assessment of S. mansoni egg excretion, perfusion and worm recovery, egg count in the liver and small intestine, percentage of egg developmental stages, and histopathological examinations. The results revealed that injection with STZ was accompanied by elevated fasting blood glucose level. Prior infection with S. mansoni significantly reduced the elevation in level of the blood glucose as a consequence of injection with STZ. Comparable numbers of worms were recovered from the two sets of infected mice. The differences in the egg load in each of the intestinal and hepatic tissues were not significant. The percentage of mature eggs was considerably higher in the nondiabetic group, while the percentage of each of immature and dead eggs was expressively greater in the diabetic set. The non-diabetic infected mice showed some histopathological alterations in the liver, small intestine and spleen. The diabetic uninfected mice exhibited some histopathological alterations in liver, spleen and pancreas. The diabetic infected mice presented significant histo-pathological variations in the liver, small intestine and spleen. It was noted that S. mansoni infection in mice relieves some of the noxious toxic effects of STZ. It was concluded that injection of mice with STZ lowers the pathology associated with S. mansoni infection and the presence of S. mansoni infection neutralizes the toxicity of STZ.
شريف رمضان عبدالغنى الرفاعى | Sherif Ramadan AbdElGhhany Elrefaey | 2897