Mucus secretion and collagen fibres integrity are compromised in aspirin induced gastric lesion; protective role of Musa paradisiaca

The study investigated the healing effects of flavonoid-rich fraction of Musa paradisiaca fruit on the gastric corpus of Wistar rats following aspirin induced-gastric lesion. Ninety adult male Wistar rats were assigned to 6 groups. Gastric lesion was induced in groups B, C, D, E and F rats by administration of 400 mg/kg aspirin. After 24 hours, the extract of M. paradisiaca was administered to groups C, D and E at graded doses for 21 days. Group F rats received omeprazole at 1.8 mg/kg daily for 21 days. The rats were sacrificed on days 14, 21 and 28. Gastric tissues were fixed in neutral buffered formalin and processed by paraffin wax embedding. Sections were stained with haematoxylin and eosin, Masson’s trichrome and periodic acid-Schiff’s. There was a gradual restoration of the damaged epithelia in the treatment groups. Histomorphometric studies revealed a significant increase in the total thickness of mucosal layers in the treatment groups when compared with aspirin only group. There was a dose-dependent improvement in staining for mucins in the treatment groups. Also, the treatment groups displayed a progressively positive stain for deposition of collagen. It is concluded that M. paradisiaca significantly attenuated the damaging effects of aspirin on the gastric mucosa, probably via a mechanism involving increase in mucin secretion

Alteration in sperm characteristics, endocrine balance and redox status in rats rendered diabetic by streptozotocin treatment: attenuating role of Loranthus micranthus

Objectives: Loranthus micranthus is widely used in Nigerian folklore treatment of male infertility and diabetes complications. We investigated this claim in rats rendered diabetic by streptozotocin (STZ). Methods: Induction of diabetes mellitus in adult male Wistar rats was by intraperitoneal injection of STZ (60 mg/kg). The diabetic rats were thereafter treated orally once/day with 5 mg/kg Gilbenclamide or L. micranthus (100 mg/kg or 200 mg/kg) and monitored for 14 days. Clinical observations, hormonal profile, oxidative stress parameters, glucose metabolism enzymes, histopathological examination, apoptotic marker immunoreactivity and western blotting in testes and sperm parameters were evaluated to examine effects of L. micranthus on STZ-diabetic rats. Results: L. micranthus treatment significantly reduced the blood glucose level (45.9% and 84.7% on the 7th and 14th post-treatment days, respectively); increased antioxidant status, improved microarchitecture of testes, reduced lipid peroxidation and increased BCl-2 protein expression in diabetic rats relative to control. Furthermore, treatment with L. micranthus increased steroidogenic enzymes activities, levels of steroid hormones and improved sperm quality, relative to control. Conclusion: The anti-diabetic and aphrodisiac properties exhibited by L. micranthus could be contingent on its ability to restore a balance to the compromised redox status that characterizes male reproductive dysfunction in diabetes

Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students

Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. Thus, optimal synaptic communication is required for proper brain physiology, and slight perturbations of synapse function can lead to brain disorders. In fact, increasing evidence has demonstrated the relevance of synapse dysfunction as a major determinant of many neurological diseases. This notion has led to the concept of synaptopathies as brain diseases with synapse defects as shared pathogenic features. In this review, which was initiated at the 13th International Society for Neurochemistry Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental disorders (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer and Parkinson disease). We finally discuss the appropriateness and potential implications of gathering synapse diseases under a single term. Understanding common causes and intrinsic differences in disease-associated synaptic dysfunction could offer novel clues toward synapse-based therapeutic intervention for neurological and neuropsychiatric disorders. In this Review, which was initiated at the 13th International Society for Neurochemistry (ISN) Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer's and Parkinson's diseases), gathered together under the term of synaptopathies