Evidence for resveratrol-induced preservation of brain mitochondria functions after hypoxia-reoxygenation.

We have previously shown, as have other authors, that trans-resveratrol (E-resveratrol, 3,4,5-trihydroxy-E-stilbene) reduces reactive oxygen species (ROS) generation of mitochondria freshly isolated from healthy rat brains and that it also counteracts the effect of uncouplers (CCCP) on mitochondrial respiration and oxidative phosphorylation. Two main mechanisms have been shown: firstly, a scavenger effect toward O2- and secondly inhibition of complex III ROS generation. We now report on the effects of resveratrol in a pathological model that mimics the ischemia followed by the reperfusion process which may occur in the human brain.

[The pharmacologic basis of pain treatment].

The treatment of chronic pain uses drugs from different pharmacological classes. Analgesics are the common basis of these treatments. Peripheral analgesics (or minor analgesics such as paracetamol) and non-steroidal anti-inflammatory drugs are used for moderate pain (grade I of WHO).

[The risk of falling due to benzodiazepine administration, alone or in combination, in elderly subjects].

Benzodiazepines are well tolerated by young adults whereas in elderly people they are less safe and globally induce more central nervous system side-effects and falls. Falls result from a decrease of vigilance and an alteration of postural reflex. This latter includes the reception of sensory information and central integration modulated mainly by dopaminergic D2 receptors and motor stimulation.

S15176 and S16950 interaction with Cyclosporin A antiproliferative effect on cultured human lymphocytes.

S15176 and S16950 are trimetazidine derivatives that antagonize more strongly than the parent drug mitochondrial toxicity, which leads to cellular hypoxia and nephrotoxicity in kidneys experimentally exposed to cyclosporin A. We have investigated whether every derivative might interact or not with the inhibitory effect of Cyclosporin A on the proliferation of cultured human lymphocytes. S15176 significantly increased the antilymphoproliferative effect of Cyclosporin A, whereas S15176 by itself neither displayed any antilymphoproliferative effect, nor did it induce any apoptotic process in cultured human lymphocytes.