BACKGROUND:5-HT1A receptors (HTR1As) in the insular cortex are thought to be related with the generation of stress-induced functional gastrointestinal disorders (FGIDs), but its mechanism is not clear. Visceral hypersensitivity is one important pathophysiological mechanism of FGIDs. This study aimed to explore the role of HTR1As in mediating stress-induced visceral hypersensitivity and its mechanism in the insular cortex.METHODS:Visceral hypersensitivity rat model was established by water avoidance stress (WAS) and the visceral sensitivity was measured by electromyogram. The activities of HTR1As were regulated by microinjecting the HTR1A agonist and antagonist into the insular cortex. The expression levels of 5-HT, HTR1A, N-methyl-d-aspartic acid receptor subtype 2B (NR2B) and c-fos were observed by RT-PCR, Western Blot and immunohistochemical staining.KEY RESULTS:In WAS rats, the expression levels of 5-HT and HTR1As in the insular cortex were significantly lower (p < 0.05) than that in sham WAS and normal rats, but the levels of c-fos and NR2B were significantly higher (p < 0.05). After microinjecting HTR1As agonist into the insular cortex of WAS rats, the visceral sensitivity and the expression levels of NR2B and c-fos in insular cortex significantly decreased (p < 0.05).CONCLUSIONS & INFERENCES:The HTR1As-NR2B signal pathway of insular cortex plays an important role in regulating stress-induced visceral hypersensitivity.

BackgroundDelayed gastric emptying (GE) is common in patients with severe burns. This study was designed to investigate effects and mechanisms of electroacupuncture (EA) on gastric motility in rats with burns.MethodsMale rats (intact and vagotomized) were implanted with gastric electrodes, chest and abdominal wall electrodes for investigating the effects of EA at ST-36 (stomach-36 or Zusanli) on GE, gastric slow waves, autonomic functions, and plasma interleukin 6 (IL-6) 6 and 24h post severe burns.Key Results(i) Burn delayed GE (P<0.001). Electroacupuncture improved GE 6 and 24h post burn (P<0.001). Vagotomy blocked the EA effect on GE. (ii) Electroacupuncture improved burn-induced gastric dysrhythmia. The percentage of normal slow waves was increased with EA 6 and 24h post burn (P=0.02). (iii) Electroacupuncture increased vagal activity assessed by the spectral analysis of heart rate variability (HRV). The high-frequency component reflecting vagal component was increased with EA 6 (P=0.004) and 24h post burn (P=0.03, vs sham-EA). (iv) Electroacupuncture attenuated burn-induced increase in plasma IL-6 at both 6 (P=0.03) and 24h post burn (P=0.003).Conclusions & InferencesElectroacupuncture at ST-36 improves gastric dysrhythmia and accelerates GE in rats with burns. The improvement seems to be mediated via the vagal pathway involving the inflammatory cytokine IL-6.

Edaravone is currently being used in acute ischemic stroke both in clinical and experimental research as a potent antioxidant. Here we explore the effects of edaravone on delayed neuronal death (DND) and long-dated cognitive dysfunction of hippocampus after cerebral ischemia-reperfusion (IR) injury and explain the underlying mechanisms and pathways. Our findings suggested that edaravone not only significantly alleviated delayed neuronal death and cognitive dysfunction of hippocampus after cerebral focal ischemia, but also markedly decreased malondialdehyde (MDA) levels. In addition, edaravone increased superoxide dismutase (SOD) levels and reduced the levels of inflammatory cytokines such as IL-1β and TNF-α expression; edaravone, also suppressed glial fibrillary acidic protein (GFAP) proliferation at days 3, 7 and 30 after reperfusion. Overall, the consensus emerging from this body of data indicated that edaravone exerts a later neuroprotective effect to hippocampus through its ability to inhibit inflammation, suppression of astrocyte activation and scavenging free radicals in stroke events.