![]() Melsungen, Germany) and was administered via an intraperitoneal ![]() The compound was freshlyĭiluted in a saline solution (0.9% NaCl B. Drugsįormaldehyde solution (37 wt% in H 2O) were obtained from Medicine and Pharmacy (Iaşi, Romania) ethical guidelines for theĮxperimental investigation of pain in conscious animals. ‘Guidelines for the use of animals in research (1991)’ ( 16) and the Grigore T. The study wasĬonducted in accordance with the European Communities Council With access to food and water ad libitum. (weight, 28–34 g), housed at 21☒☌ under a 12-h light/dark cycle, Materials and methods AnimalsĮxperiments were conducted on 80 male BALB/c mice Nociception and locomotor activity in mice. The aim of the present study was to investigate theĮffects of modulating mitochondrial function and cellularĪntioxidant capacity by CoCl 2 preconditioning on Hyperalgesia and in antinociceptive tolerance ( 14). Transition from acute to chronic pain, in opiate-induced Member of the ROS family produced during hypoxia, and mitochondrialĪctivation, are involved in the development of chronic pain, in the There is increasing evidence that superoxide, a Indicates that CoCl 2 preconditioning has Mitochondrial biogenesis, glucose uptake and metabolism in theĪttenuates vascular leakage and ROS-induced hypoxia generation in (CoCl 2) activates hypoxia-inducible factor (HIF)-1α,Īcting as a hypoxia-mimetic and inducing reactive oxygen speciesįurthermore, CoCl 2 is able to stabilize HIF-1α, a keyĭeterminant of the cellular response to hypoxia, which has made theĬompound one of the most commonly used hypoxia-mimetic agentsĭemonstrated that CoCl 2 preconditioning increases That Co can cause memory impairment ( 6).Ī previous study indicated that Co chloride Including dopamine, norepinephrine and serotonin, which suggests Has been shown to induce a depletion of neurotransmitters, Inhibitory effects on Ca 2+ signaling ( 5). Intracellular Ca 2+-binding proteins and thus exerting ![]() Co has also been hypothesized toįunction as a Ca 2+ channel antagonist, competing for Inhibiting synaptic transmission through the presynaptic blockage To decrease neurotransmitter-induced postsynaptic responses by To its high affinity for sulfhydryl groups ( 3). Leads to mitochondrial swelling and electrical membrane potentialĮnzymes that participate in the mitochondrial respiratory chain due Mitochondrial permeability by opening the transition pores, which Previous studies have demonstrated that Co modifies The mechanism by which Co acts on cells isĬontroversial. Hemoglobin concentrations and congestive heart failure, due to theĪddition of Co sulfate to the beer as a stabilizer ( 1). The toxic effect of Co wasįirst described in 1966, when beer drinkers developed aĬardiomyopathy characterized by pericardial effusion, elevated Thus, the present study demonstrated that CoCl2 preconditioning has a dual effect on pain, and these effects should be taken into account along with the better‑known neuro‑, cardio‑ and renoprotective effects of CoCl2.Ĭobalt (Co) is a ferromagnetic transition metal,Įssential to human health, that plays a critical role in the The first phase of formalin‑induced pain and the writhing test were not affected by CoCl2 preconditioning. Contrary to the hyperalgesic effect on thermonociception, CoCl2 hypoxic preconditioning decreased the time spent grooming the affected area in the second phase of the formalin test on the orofacial and paw models. Thermal hyperalgesia (Plantar test) was present in the first week, but recovered by the end of the experiment. A significant pronociceptive effect was observed in the hot plate and tail flick tests after one and two weeks of CoCl2 administration, respectively (P<0.001). The aim of the present study was to investigate the effects of CoCl2 hypoxic preconditioning for three weeks on thermonociception, somatic and visceral inflammatory pain, locomotor activity and coordination in mice. Cobalt chloride (CoCl2) modifies mitochondrial permeability and has a hypoxic‑mimetic effect thus, the compound induces tolerance to ischemia and increases resistance to a number of injury types.
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