The K(ATP) channels may play an important role in the gastric mucosal restitution independent of polyamines. Acid inhibition cannot reverse EAGU.
As a cancer chemotherapeutic agent, paclitaxel (Taxol Ò ) causes dose-related peripheral neuropathy in human beings. The mechanisms underlying this toxicity are currently unknown, and there are no validated treatments for its prevention or control. To assess whether lithium as a pre-treatment and at subtherapeutic dose could prevent the peripheral neuropathy produced by it, rats were treated with paclitaxel (2 mg ⁄ kg i.p. every other day for a total of 16 times) and ⁄ or lithium chloride (300 mg ⁄ l) via water supply. General toxicity and body-weight were measured regularly during the experiment. To evaluate the sensory and motor neuropathy hot-plate, open-field test and nerve conduction velocity were used. In rats treated with only paclitaxel, there was behavioural, electrophysiological and histological evidence of a mixed sensorimotor neuropathy after 16 injections. Lithium robustly reduced the rate of mortality and general toxicity. Paclitaxel-induced sensorimotor neuropathy was significantly improved as indicated by changes in hotplate latency, total distance moved and a significant increase in sciatic, sural and tail sensory or motor nerve conduction velocity. The same results were observed in histopathological examinations; however, dorsal root ganglion neurons did not significantly change in the paclitaxel-treated groups. These results suggest that lithium, at subtherapeutic doses, can prevent both motor and sensory components of paclitaxel neuropathy in rats. Thus, lithium at these doses, as an inexpensive and relatively safe salt, may be useful clinically in preventing the neuropathy induced by paclitaxel treatment.Paclitaxel is an effective anti-tumour agent initially isolated from the bark of the pacific yew tree, Taxus brevifolia, and is regularly used to treat long, ovarian cancer either by itself or in combination with other anti-tumour agents [1][2][3]. Paclitaxel causes excessive tubulin polymerization leading to mitotic arrest and thus inducing apoptosis in dividing cells [4].Microtubules play an important role in cellular functions such as membrane and cellular scaffolding, intracellular transport of organelles or proteins and transmission of signals initiated at cell surface receptors. Thus, microtubules interfering agents like vincristine or paclitaxel may disturb non-neoplastic cells such as nerves and finally cause apoptosis. Hence, peripheral neuropathy is one of the most frequent side effects of these two drugs that usually result in dose modification and changes in the treatment plan [5][6][7][8].As a mood stabilizer, lithium is commonly prescribed for bipolar disorders, and although its mechanism of action remains unknown, it is well established that lithium exerts some of its therapeutic effects through G-protein-coupled pathway, glycogen synthase kinase-3 (GSK3b), inositol monophopsphate and nitric oxide-dependent pathways and augmentation of serotonin function in the central nervous system [9,10]. Previous studies have reported that lithium has neuroprotective effects. The...
Leonurus cardiaca, commonly known as motherwort, is a member of the Lamiaceae family. It has a number of interesting biological activities, for example, sedative and hypotensive, antioxidant, anti-inflammatory, and antimicrobial activities. The aim of the present study was to investigate the effect of alcoholic extract of aerial part of Leonurus cardiaca on nociceptive response using formalin, tail flick, and hot plate tests in mice. The acute treatment of mice with an ethanolic extract at doses of 500 and 250 mg/kg by intraperitoneal administration produced a significant antinociceptive in the first and second phases of formalin test, respectively. The hot plate and tail flick tests showed an increase in the antinociceptive effect at dose 500 mg/kg. These results suggest that Leonurus cardiaca possesses central and peripheral antinociceptive actions.
It has been proposed carbon tetrachloride (CCl 4 ) intoxication due to the production of free radicals and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) overload results hepatotoxicity. Phosphatidylserine (PS) has shown antioxidant activity in numerous studies.Therefore, this study was aimed to investigate the effects of PS liposomes treatment against the CCl 4 -induced hepatotoxicity in a rat model. Male Wistar rats were treated with PS (10 mg/kg, oral) or phosphatidylcholine liposomes (PC) (10 mg/kg, oral) for 3 days before CCl 4 (2 ml/kg; ip once on the third day) injection. The serum level of ALT, AST, and ALP were measured. Also, antioxidant assays were performed.Administration of PS with CCl 4 significantly inhibited alterations in the serum levels of AST, ALP ( ** P < 0.01), and ALT ( *** P < 0.001) compared with control group. Furthermore, measurement of malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels indicated that PS significantly reduced reactive oxygen species. The results of the present study showed the hepatoprotective effects of PS against CCl 4 -induced hepatotoxicity in rats. K E Y W O R D Santioxidant, CCl 4 , hepatoprotective, liposome, phosphatidylserine
Based on our previous demonstration of the involvement of dopamine-2 (D2) dopamine receptors in morphine antinociception, we examined the role of D2 dopamine receptors in the expression and development of tolerance to morphine antinociception in mice. Tolerance to morphine antinociception was assessed by the tail-flick response after the administration of morphine (50 mg/kg) once daily for 3 days. The D2 dopamine receptor agonist, quinpirole (0.01, 0.02 and 0.03 mg/kg), but not the D2 dopamine receptor antagonist, sulpiride (12.5, 25 and 50 mg/kg), increased morphine antinociception in morphine non pre-exposed mice. The response of quinpirole was decreased by the lower doses of sulpiride. Both quinpirole and sulpiride decreased the expression and development of tolerance to antinociception induced by morphine (1.5, 3 and 6 mg/kg). The effect of quinpirole on the expression and development of tolerance, was reduced by a lower and per se non-effective dose of sulpiride. It was concluded that D2 dopaminergic receptors may play a part in the expression and development of tolerance to the antinociceptive effect of morphine.
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