Melissa officinalis acidic fraction protects cultured cerebellar granule neurons against beta amyloid-induced apoptosis and oxidative stress

Objective: Extracellular deposition of the beta-amyloid [A beta] peptide, which is the main finding in the pathophysiology of Alzheimer's disease [AD], leads to oxidative damage and apoptosis in neurons. Melissa officinalis [M. officinalis] is a medicinal plant from the Lamiaceae family that has neuroprotective activity. In the present study we have investigated the protective effect of the acidic fraction of M. officinalis on A beta-induced oxidative stress and apoptosis in cultured cerebellar granule neurons [CGN]. Additionally, we investigated a possible role of the nicotinic receptor

Materials and Methods: This study was an in vitro experimental study performed on mice cultured CGNs. CGNs were pre-incubated with different concentrations of the acidic fraction of M. officinalis for 24 hours, followed by incubation with A beta for an additional 48 hours. CGNs were also pre-incubated with the acidic fraction of M. officinalis and mecamylamin, followed by incubation with A beta. We used the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide [MTT] assay to measure cell viability. Acetylcholinesterase [AChE] activity, reactive oxygen species [ROS] production, lipidperoxidation, and caspase-3 activity were measured after incubation. Hochst/annexin V- fluorescein isothiocyanate [FITC]/propidium iodide [PI] staining was performed to detect apoptotic cells

Results: The acidic fraction could protect CGNs from A beta-induced cytotoxicity. Mecamylamine did not abolish the protective effect of the acidic fraction. AChE activity, ROS production, lipid peroxidation, and caspase-3 activity increased after A beta incubation. Pre-incubation with the acidic fraction of M. officinalis ameliorated these factors and decreased the number of apoptotic cells

Conclusion: Our results indicated that the protective effect of the acidic fraction of M. officinalis was not mediated through nicotinic receptors. This fraction could protect CGNs through antioxidant and anti-apoptotic activities

Responses of serum calcium and inorganic phosphate levels, parathyroid gland and C cells of Rattus norvegicus to heptachlor administration.

Intramuscular administration of two doses: 0.50 LD50 (14.70 mg/kg b w) and 0.75 LD50 (22.30 mg/kg b w) of heptachlor in Rattus norvegicus for 14 days induced significant hypocalcemia without altering serum inorganic phosphate value. Parathyroid chief cells of the experimental rats exhibited degranulation, vacuolation, loss of secretory granules and lipid droplets, reduction in chromatin, and degenerative changes in endoplasmic reticulum and cristae of the mitochondria. Not much of histological and ultrastructural changes could be seen in C cells of the heptachlor treated rats.

Physiology and function of platelets from patients with Alzheimer's disease.

The discovery that intact Alzheimer amyloid precursor protein is present in platelet granules, has created a great interest in the biochemistry, physiology and function of platelets of patients with Alzheimer disease (AD). In this study we monitored various biochemical and physiological parameters, such as serotonin and adenine nucleotide levels, membrane fluidity, agonist-mediated release of arachidonic acid, thromboxane formation, calcium mobilization, as well as irreversible aggregation and secretion of granule contents. Platelets of patients with AD responded poorly when stirred with weak or potent agonists on a platelet aggregometer. Although capable of agonist-mediated calcium mobilization and synthesis of thromboxanes, the aggregation response of platelets of patients with AD to thrombin and archidonate was considerably compromised. In view of the normal biochemistry and signal transduction capabilities, the compromised response of these cells to potent agonists like thrombin suggested an extrinsic defect. The present study has shown that a plasmatic factor is at least in part responsible for the functional abnormalities of AD platelets.

Effect of cyproheptadine on glucose tolerance, serum insulin and structure of pancreatic islets in rats.

The effect of cyproheptadine (CPH) on glucose tolerance, serum immunoreactive insulin (IRI) and structure of pancreatic islets in albino rats has been studied. Hyperglycemia with glucose intolerance was observed after 10 days of administration of CPH (40 mg/kg, ip). There was insignificant change of fasting IRI after the treatment. Histological studies indicated degranulation and vacuolation of beta cells with enlargement of capillaries. Improvement in blood glucose, glucose tolerance and structure of islets with proliferation of small pancreatic ducts and cell cords were observed 10 days after the withdrawal of CPH.

Electron Microscopic Observations on the Morphological Changes of Rat Mesentric Mast Cells Induced by Morphine HCl

The effects of morphine HCI on the rat mesenteric mast cells were studied with the electron microscopy. The materials were prepared for electron microscopy by osmium tetroxide fixation and embedding in Epon. The rat mesenteric mast cells showed no distinct morphological changes due to morphine HCl, but the mast cell granlues were changed in various ways. For instance, they formed dusters, showed granular lysis, and an appearance of electron transparency. Frequently, some granules appeared in the extracellular space and the boundary of the granules was not evident. From the results mentioned above, it was suggested that rat mesenteric mast cell granules were affected by morphine HCl in the shape, the granular matrix, and the granular boundaries.

Mast Cell Degranulation with Special Reference to the Effect of Lipid Administration upon the Mesenteric Mast Cell of Albino Rats

Morphological effects of degranulation upon me-senteric mast cells of albino rats (SPrague-Dawley strain) by means of lipid administration were studied. An evident degranulation of metachromatic granules from mesenteric tissue mast cells was observed in more than half of experimental rats which were intraperitoneally given 10cc of stearic monoglyceride suspension in warm Tyrode solution (5Omg. of stearic monoglyceride in 10cc of Tyrode solution). A fairly light degranulation of metachro-matic granules from mesenteric mast cells was also displayed by the rats fed ad libitum with butter for 6 hours after being deprived of food for 24 hours.