Our study demonstrated that Mentha piperita has inhibited the initiation and promotion of oral dysplastic lesions.
We induced hypothyroidism (HT) in male rats through chronic oral administration of carbimazole and then tested whether an i.v. injection of rat bone marrow-derived mesenchymal stem cells (BM-MSCs) could ameliorate the HT-induced changes in pancreatic structure and function. The thyroid and pancreatic function tests, as well as total antioxidant capacity (TAC) and malondialdehyde (MDA) were estimated. The pancreatic structure was evaluated by hematoxylin and eosin (H&E) stain. Insulin protein and cleaved caspase-3 were detected immunohistochemically. The degree of apoptosis was assessed by TUNEL assay. The morphometric measurements were done by an image analyzer system and the obtained data were statistically analyzed. HT rats showed hyperglycemia associated with insulin deficiency, decreased TAC and increased MDA levels. H&E-stained sections showed that the pancreatic septa were infiltrated with acidophilic material. Some acini were vacuolated while others showed depleted acidophilia and dilated lumina. Spindle-shaped cells were accumulated within deformed islets in HT rats. The positive reaction with anti-cleaved caspase-3 was exclusively noted in the cytoplasm of islet cells with no immunostaining reaction in the acinar and ductal cells, whereas the positively stained nuclei with TUNEL were demonstrated in the islet and acinar cells. A significant increase in the apoptotic index % of both markers was detected. Injection of BM-MSCs in HT rats restored all biochemical indicators of disturbed pancreatic function to normal level and improved pancreatic structure, resulting in a clear septa and normal appearance of acini and islets. In conclusion, many of the significant structural and func tional pancreatic alterations detected in HT rats were ameliorated after the injection of BM-MSCs. These data demonstrate the ability of BM-MSCs to repair pancreatic disturbances. Further studies on humans are necessary to determine the potential clinical applications of BM-MSCs.
Hypoglycemia is a neglected metabolic disorder. Thus, we evaluated the protective effect of hypoxia-preconditioned human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) on hypoglycemic testicular injury. We examined 56 testes from 28 animals: 7 rats with insulin-induced hypoglycemia (HG group), 7 hypoglycemic rats which received an intratesticular injection of hUCB-MSCs (HG-MSC group), and 14 untreated control rats. Testosterone level, testicular catalase (CAT) activity, and malondialdehyde (MDA) level were analyzed. Immunostaining for specific testicular germ and somatic cell markers was performed. Proliferating and apoptotic cells were detected by anti-PCNA and anti-caspase-3, respectively. Morphometrical data were statistically analyzed. The hypoglycemic rats showed a significant decrease in testosterone level and CAT activity and a significant increase in MDA production. Examination of histological structure and protein expression of diverse germ cell markers revealed collapsed tubules that were lined by degenerated germ cells, decreased lactate dehydrogenase type C immune expression, as well as decreased proliferating and increased apoptotic cells number in hypoglycemic testes. Injection of MSCs improved testicular biochemical parameters, preserved germ cells and somatic cells, and decreased apoptosis. In conclusion, hypoxia-preconditioned hUCB-MSCs attenuate rat testicular injury caused by insulin-induced hypoglycemia. Avoidance and rapid management of hypoglycemia are necessary to avoid significant testicular injury.
Background: Levetiracetam is a broad-spectrum antiseizure agent and one of the most commonly prescribed drugs for epilepsy. The aim of this work was to assess the effect of levetiracetam at its therapeutic range on the liver and kidney of pregnant albino rats. Materials and methods: Forty pregnant rats were divided equally into two groups (I-II), Rats in the group I were gavaged 1.5 mL/day distilled water in two divided doses throughout pregnancy. Rats in the group II were gavaged 1.5 mL/day distilled water (containing 36 mg levetiracetam) in two divided doses throughout pregnancy. At the end of the experiment, blood samples were taken and the sera were separated and used for biochemical analysis. The kidneys and livers of both groups were excised and used for light and electron microscopic examination. Results: Treatment with levetiracetam induced undesirable histopathological changes in the liver and kidney of pregnant albino rats. These changes were in the form of distortion of the hepatic architecture, dilatation of the central and the portal veins, widening of the Bowman's spaces, thickening and disruption of the glomerular basement membrane, fusion and effacement of secondary foot processes, cytoplasmic vacuolation, and swollen mitochondria with loss of their cristae. Such changes were confirmed by alteration of certain biochemical parameters related to the liver and kidney functions. Conclusions: Levetiracetam induced deleterious effects on the liver and kidney of pregnant albino rats. Further investigations are recommended to clarify the mechanism of levetiracetam toxicity. (Folia Morphol 2019; 78, 4: 809-817)
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