Detail of "188817-13-2"

Reference

Nonsteroidal Anti-Inflammatory Drugs Can Lower Amyloidogenic Ab42 by Inhibiting Rho

Nonsteroidal Anti-Inflammatory Drugs Can Lower Amyloidogenic Ab42 by Inhibiting Rho. Zhou, Yan; Su, Yuan; Li, Baolin; Liu, Feng; Ryder, John W.; Wu, Xin; Gonzalez-DeWhitt, Patricia A.; Gelfanova, Valentina; Hale, John E.; May, Patrick C.; Paul, Steven M.; Ni, Binhui (Lilly Research Laboratories, Neuroscience Discovery Research and Bioresearch Technologies and Proteins, Eli Lilly and Company, Indianapolis, IN 46285, USA). Science (Washington, DC, United States), 302(5648), 1215-1218 (English) 2003 American Association for the Advancement of Science. CODEN: SCIEAS. ISSN: 0036-8075. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) A subset of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to preferentially reduce the secretion of the highly amyloidogenic, 42-residue amyloid-b peptide Ab42. We found that Rho and its effector, Rho-assocd. kinase, preferentially regulated the amt. of Ab42 produced in vitro and that only those NSAIDs effective as Rho inhibitors lowered Ab42. 188817-13-2 and 182372-13-0 which are cas registry numbers of substances are two of reagents here. Administration of Y-27632, a selective Rock inhibitor, also preferentially lowered brain levels of Ab42 in a transgenic mouse model of Alzheimer's disease. Thus, the Rho-Rock pathway may regulate amyloid precursor protein processing, and a subset of NSAIDs can reduce Ab42 through inhibition of Rho activity. .

Effects of Selective Cyclooxygenase Inhibitors on Ischemia/Reperfusion-Induced Hepatic Microcirculatory Dysfunction in Mice

Effects of Selective Cyclooxygenase Inhibitors on Ischemia/Reperfusion-Induced Hepatic Microcirculatory Dysfunction in Mice. Ito, Y.; Katagiri, H.; Ishii, K.; Kakita, A.; Hayashi, I.; Majima, M. ( Department of Surgery, Kitasato University School of Medicine, Sagamihara, Japan). European Surgical Research, 35(5), 408-416 (English) 2003 S. Karger AG. CODEN: EUSRBM. ISSN: 0014-312X. DOCUMENT TYPE: Journal CA Section: 14 (Mammalian Pathological Biochemistry) Section cross-reference(s): 1 We examd. 188817-13-2 and 329900-75-6 are cas registry numbers of chemicals which are used as reagents here. the effects of selective cyclooxygenase (COX) inhibition on hepatic warm ischemia/reperfusion (I/R) injury in mice. A selective COX-1 inhibitor, SC-560, selective COX-2 inhibitors, NS-398 and celecoxib, and indomethacin were administered 30 min before ischemia. Four hours after reperfusion, an in vivo microscopic study showed that I/R caused significant accumulation of leukocytes adhering to the hepatic microvessels and nonperfused sinusoids. Levels of plasma alanine transaminase (ALT) and tumor necrosis factor (TNF)-a also showed increases. SC-560, NS-398, celecoxib and indomethacin significantly reduced hepatic responses to I/R including microcirculatory dysfunction and release of ALT and TNF-a. Moreover, the effects of the thromboxane (TX) A2 (TXA2) synthase inhibitor OKY-046 and the TXA2 receptor antagonist S-1452 on hepatic responses to I/R exhibited results similar to those obtained with COX inhibitors. These results suggest that COX-1 and COX-2 contribute to I/R-induced hepatic microvascular and hepatocellular injury partly through TNF-a prodn., and that TXs derived from COX are partly responsible for I/R-induced liver injury. .