Detail of "189388-22-5"

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Paradoxical hyperalgesia induced by m-opioid receptor agonist endomorphin-2, but not endomorphin-1, microinjected into the centromedial amygdala of the rat

All Rights Reserved. Paradoxical hyperalgesia induced by m-opioid receptor agonist endomorphin-2, but not endomorphin-1, microinjected into the centromedial amygdala of the rat. Terashvili, Maia; Wu, Hsiang-En; Schwasinger, Emma; Tseng, Leon F. (Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA). European Journal of Pharmacology, 554(2-3), 137-144 (English) 2007 Elsevier B.V. CODEN: EJPHAZ. ISSN: 0014-2999. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 1 The effects of endomorphin-2 or endomorphin-1 microinjected into the centromedial amygdala on the thermally-induced tail-flick response were studied in male CD rats. Microinjection of endomorphin-2 (8.7-35.0 nmol) given into the centromedial amygdala time- and dose-dependently decreased the tail-flick latencies. On the other hand, endomorphin-1 (8-32.6 nmol) given into the same site did not cause any change of the tail-flick latency. However, endomorphin-1 (32.6 nmol) or endomorphin-2 (35.0 nmol) given into the basolateral site of amygdala did not affect the tail-flick latency. Pretreatment with the antiserum against dynorphin A(1-17) (200 mg) significantly reversed the decrease of the tail-flick latency induced by endomorphin-2. 80448-90-4 and 189388-22-5 are also in the experiment. The decrease of the tail-flick latency induced by endomorphin-2 was also blocked by the endomorphin-2 selective m-opioid receptor antagonist 3-methoxynaltrexone (6.4 pmol) and by the N-methyl--aspartate (NMDA) receptor antagonist MK-801 (30 nmol), but not by the k-opioid receptor antagonist nor-binaltorphimine (6.6 nmol). It is concluded that endomorphin-2, but not endomorphin-1, given into the centromedial amygdala stimulates a 3-methoxynaltrexone-sensitive m-opioid receptor subtype to induce the release of dynorphin A(1-17), which then acts on the NMDA receptor, but not k-opioid receptor for producing hyperalgesia. This conclusion is further supported by the addnl. findings that dynorphin A(1-17) (2.3 nmol) given into the centromedial amygdala also caused the decrease of the tail-flick latency, which was similarly blocked by the NMDA receptor antagonist MK-801 (30 nmol), but not k-opioid receptor antagonist nor-binaltorphimine (6.6 nmol). .

Endomorphins, endogenous opioid peptides, induce apoptosis in human leukemia HL-60 cells

Endomorphins, endogenous opioid peptides, induce apoptosis in human leukemia HL-60 cells. Lin, Xin; Chen, Qiang; Xue, Li-Ying; Ma, Xiao-Jun; Wang, Rui ( Department of Biochemistry and Molecular Biology, School of Life Science, Lanzhou University, Lanzhou 730000, Peop. Rep. China). 141801-26-5 and 189388-22-5 are cas registry numbers. These chemicals are also mentioned in this article. Canadian Journal of Physiology and Pharmacology, 82(11), 1018-1025 (English) 2004 National Research Council of Canada. CODEN: CJPPA3. ISSN: 0008-4212. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 14 Opioids play a role in the apoptosis machinery. We studied the induction of apoptosis in endomorphin 1 (EM1) and endomorphin 2 (EM2), 2 newly isolated endogenous m-opioid receptor agonists. These endomorphins were able to reduce the viability of cultured HL-60 cells. The antiproliferative properties of endomorphins appeared to be attributable to their induction of apoptotic cell death as detd. by ultrastructural change, internucleosomal DNA fragmentation, and increased proportion of the subdiploid cell population. To elucidate mol. events in the apoptosis, protein expressions of Bcl-2, Bax, Fas, and FasL were measured by western blotting using specific antibodies in HL-60 cells. The level of Bcl-2 indicated down-regulation, but the Bax, Fas, and FasL expression showed up-regulation as compared with the untreated control cells. These data support the idea that endomorphins induce apoptosis in HL-60 cells through the activation of the Bcl-2-Bax and the Fas-FasL pathway. We suggest that endomorphins may play an important role in the regulation of tumor cell death. .