Protective Effect of Capsaicin on the Ischemia-Reperfusion Injury of the Intestine in Rats

PURPOSE: Capsaicin, a major ingredient of hot peppers, has a stimulatory effect on the neurons. Ingested capscaicin causes pain and even damages the mucosa with a large dose. On the other hand, it protects the gastric mucosa against many ulcerogenic agents or conditions. In this study, we investigated the effect of oral capsaicin on the ischemia-reperfusion damage of the intestinal mucosa in rats. The involvement of stress proteins such as HSP-70 and HSP-72 in the action of capsaicin was also investigated. METHODS: Male Sprague-Dawley rats were given oral capsaicin (20 mg/kg/day) for a designated period. Ischemia of the small intestine was inflicted by clamping the superior mesenteric arteries for 30 minutes under anesthesia. After the ischemic period, the clamp was released and the animal was kept for 1, 5, or 24 hours. Then, the intestinal structure was observed under the microscope, and the levels of the heat-shock proteins were determined by using a Western blot. RESULTS AND CONCLUSION: Oral capsaicin protected the mucosa of the small intestine against the ischemia/reperfusion injury. Capsaicin also increased and expedited the ischemia/reperfusion-induced expression of the heat-shock proteins, HSP-70 and 72, in the intestine. The possible linkage between the two events is discussed.

beta-amyloid Peptides Induced Neuronal Apoptosis without Tau Phosphorylation / 대한해부학회지

beta-amyloid peptide (Abeta) consisting of 40 to 42 amino acid is the principle constituent of senile plaques in Alzheimer's disease. Although, the hypothesis that deposition of AP triggers a cascade of events leading to the pathology of Alzheimer's disease has been widely accepted, direct evidence for triggering accumulation of phosphorylated tau in paired helical filament is rare. In this study, we examined neurotoxicity induced by 3 kinds of beta-amyloid peptides 1 ~28, 25~,35 and 1~40 to elucidate the way of mechanism trading to neuronal cell death caused by Abeta using cultured hippocampal neurons. For this purpose, we measured lactate dehydrogenase (LDH) in the culture media after treatment with Abeta combined with anti-oxidant drug, trolox, or not. By histochemical and TUNEL method, we studied the change of immunoreaction to anti-MAP-2 (microtubule associated protein -2, the main component of neuritis) and detected apoptotic cells, respectively, in the hippocampal neurons treated with Abeta. To investigate whether tau phosphorylation involve neurotoxicity induced by Abeta, we immunostained the neurons with anti-SMI-31 to recognize phosphorylated Ser 396/404 of tau. From our data, we suggested that Abeta1-40 and Abeta25-35 induced marked neurodegenerative changes, and the mechanism responsible for cell death caused by Abeta -neurotoxicity was associated with the apoptosis. Because Abeta-neurotoxicity was not inhibited by anti-oxidant, trolox, we suggested that anti-oxidant did not protect the neuronal cells against the damage induced by Abeta in ou. expo.imental envi.onment. Finally, we suggested that AP treatment did not potentiate the immunoreactivity to anti-phosphorylated tau antibody and we speculated that Abeta-neurotoxicity led hippocampal cells to apoptosis without tau phosphorylation.

P MR spectroscopy study of the brain at 4.7 T in new borns

In vivo 31P NMR spectra were obtained in eight infant brain at 4.7T. Each phosphorus metabolite and its ratio were analyzed to evaluate the brain damage and maturity, and compared with the reported data obtained at the lower field strength. Measurement of T1 relaxation time at 4.7T was done in an infant and a cat brain in vivo. PCr/Pi and PCr/β-ATP ratio were used as a marker of brain damage. PME/PDE revealed higher values than those of the reported data obtained at the lower field strength and the difference was partly attributed to the long T1 relaxation time of PME rather than the brain immaturity. Although the resolution of the spectrum was improved at 4.7T, a long repetition time is recommended to minimize T1difference of phosphorus metabolites of brain at 4.7T.