Brain research
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Comparative Study
Involvement of peripheral opioid receptors in electroacupuncture analgesia for carrageenan-induced hyperalgesia.
Acupuncture is widely used to relieve pain; however, the mechanism underlying electroacupuncture analgesia (EAA) during inflammatory pain is unclear. We investigated whether endogenous peripheral opioid receptors participated in EAA during hyperalgesia elicited by carrageenan-induced inflammation. Moreover, we investigated which subtype of opioid receptor was involved in EAA. ⋯ NTI, nor-BNI and CTOP blocked EAA from immediately, 1h, and 3h after EA cessation, respectively. The EAA in the inflamed paw could not be blocked by i.v. injection of NTI, nor-BNI and CTOP. These findings suggest that peripheral μ, δ and κ receptors on peripheral nerve terminals are activated by EA, although there is a time difference among these activations.
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Many studies have demonstrated the anti-nociceptive and anti-inflammatory effects of injecting bee venom (BV) into the Zusanli (ZSL) acupoint in rats. The present study was designed to determine whether the injection of other chemical irritants, such as formalin and complete Freund's adjuvant (CFA), into the ZSL acupoint can produce anti-nociceptive and anti-inflammatory effects in the BV pain model and to determine the possible mechanisms underlying these effects. First, the effects of injecting BV, formalin, CFA, or saline into the ZSL acupoint on intraplantar BV-induced persistent spontaneous pain, mechanical hyperalgesia, and inflammatory swelling of the injected paw were observed. ⋯ Pretreatment with capsaicin produced partial blockage of the BVA-induced anti-nociceptive effect on PSN, but it had no effect on BVA-induced anti-nociception of mechanical hyperalgesia. These results suggest that (1) chemical irritant acupuncture produces the anti-nociceptive effect but not the anti-inflammatory effect in the BV pain model, and (2) chemical irritant acupuncture-induced analgesia is a common mechanism that is not specific to BV acupuncture. Our results also suggest that the BVA-induced anti-nociceptive mechanism is partially mediated by capsaicin-sensitive primary afferent fibers but not by endogenous mu opioid receptors in the BV pain model.
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Traumatic brain injury (TBI) is a leading cause of mortality and disability among the young population. It has been shown that hydrogen gas (H(2)) exerts a therapeutic antioxidant activity by selectively reducing hydroxyl radical (OH, the most cytotoxic ROS). Recently, we have found that H(2) inhalation significantly improved the survival rate and organ damage of septic mice. ⋯ Here, we found that TBI-challenged rats showed significant brain injuries characterized by the increase of BBB permeability, brain edema and lesion volume as well as neurological dysfunction, which was significantly attenuated by 2% H(2) treatment. In addition, we found that the decrease of oxidative products and the increase of endogenous antioxidant enzymatic activities in the brain tissue may be associated with the protective effects of H(2) treatment in TBI-challenged rats. The present study supports that H(2) inhalation may be a more effective therapeutic strategy for patients with TBI.
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Sepsis and septic shock are the commonest causes of death in the intensive care units. Although recent research have improved our understanding of the progress and pathophysiology of sepsis and septic shock, underlying mechanisms in sepsis-associated encephalopathy is still poorly understood. The incidence of sepsis-associated encephalopathy has been reported to vary from 8% to 70% of septic patients. ⋯ Significant decrease in mean arterial pressure, increase in heart rate, deteriorated neurological reflexes together with positive blood cultures results, thrombocytopenia and increased blood lactate levels suggesting the successful induction of sepsis in the present study. Elongated latencies and increased amplitudes were observed in somatosensory recordings of septic group, while electrocorticograms revealed slight decrease in median and spectral edge frequencies amplitudes and significantly increased delta activities in 50% of the septic rats. These results would suggest that the studies based on the investigation of the sepsis-associated encephalopathy in animal models needs to be combined with the electrophysiological confirmations of the brain dysfunction following the induction of sepsis.