hooman bozorgi

 Morphine withdrawal syndrome is often treated with chemical drugs; however, these drugs can have concerning side effects. Some natural substances might offer safer alternatives for managing withdrawal symptoms. The neuroprotective activity of the adenosine A1 receptor (A1R) in the central nervous system (CNS) has been mentioned before. As a novel natural agent, Japanese sake yeast is enriched with adenosine analogs.

 As the first report, the present study was designed to evaluate the effects of the Japanese sake yeast supplement against the excitatory signs of morphine withdrawal syndrome in mice.

 Mice were treated orally (gavage) with sake yeast at doses of 100, 200, and 300 mg kg-1 once daily for a week. Furthermore, during the last 3 days of receiving sake yeast, the animals were made physically dependent on morphine by being given twice-daily subcutaneous injections of increasing doses of morphine (30 - 90 mg/kg) for 3 consecutive days. The withdrawal syndrome was induced in animals through the intraperitoneal (i.p.) administration of naloxone (3 mg kg-1) or was elicited spontaneously. After the examination of withdrawal signs, the animals were decapitated, and their brains were prepared for histopathology.

 Sake yeast alleviated the intensity of ptosis, piloerection, diarrhea, irritability, and tremor during the two withdrawal syndrome protocols (P < 0.05) and diminished the number of jumping in naloxone-induced withdrawal syndrome (P < 0.01). The withdrawal symptom-lowering effect of sake yeast was reversed by the i.p. injection of an A1R-selective antagonist, 8-cyclopentyltheophylline (10 mg kg-1), and maintained following the i.p. injection of ZM241385 (15 mg kg-1), a selective adenosine A2AR antagonist. Furthermore, histopathological findings demonstrated that sake yeast at doses of 200 and 300 mg kg-1 inhibited the CA1 hippocampal neuronal damage induced by withdrawal syndrome (P < 0.05).

 Sake yeast suppresses the morphine withdrawal syndrome via the activation of A1R.

 Alzheimer disease (AD) is the most common type of dementia in the elderly. Memory impairment usually occurs gradually and progressively. AD has not only been associated with decreased cerebral acetylcholine concentration, oxidative stress, and beta-amyloid protein deposition, but more recent studies have shown that neurodegeneration induced by disturbance of the intracellular calcium homeostasis is also involved in the pathophysiology of the disease. It has been reported that calcium channel blockers (CCBs) have beneficial effects in different models of memory impairment. Here, we review and discuss the effects of CCBs, especially N-types, as novel agents that have effects on memory deficits in animal models of AD. on contrary to the L-type calcium channels, which are presented in the other organs in addition to nerve cells, N-type calcium channels are commonly located on the neurons. The main advantage of N-type CCBs is their lower side effects than other CCBs.

Targeting the N-type CCBs may contribute to the new strategies for the treatment of AD.

To evaluate the effect of tetracaine on intraocular pressure (IOP) in normal and hypertensive rabbit eyes. The study was conducted on 12 healthy rabbits as controls and 6 healthy rabbits in which an experimental model of ocular hypertension (OHT) was induced by administration of 70 mL/kg of tap water through an orogastric tube. One drop of tetracaine was instilled in the left eye while a drop of normal saline (placebo) was applied to the right eye of the control group. IOP was measured before and 0, 5, 10,15, 20, 25, 30, 35 and 40 minutes after drop administration in this group. The OHT group also received one drop of tetracaine and normal saline in the left eyes and right eyes respectively, immediately after water loading; the instillation of drops was repeated after 55 minutes. IOP was measured before and 0, 5, 10, 15, 20, 25, 30, 35,40, 55, 70, 85, 100 and 115 minutes after water loading in this group. Tetracaine treated eyes in both groups (ocular hypertensive and normal controls) demonstrated significant IOP reduction at time zero (immediately after drop instillation) which was sustained up to 20 minutes, as compared to placebo treated eyes (P)