PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9797040-4 1998 Troglitazone also reduces interleukin-1alpha induced nitric oxide production in pancreatic beta-cells, which may be relevant in preventing nitric oxide mediated damage to these cells in the Type 1 diabetes process. Nitric Oxide 53-65 interleukin 1 alpha Mus musculus 26-44 25047145-9 2014 In addition to the loss of GAGs and tissue mechanical properties, IL-1alpha treatment induced the expression of matrix metalloproteinases and increased the production of the inflammatory mediators nitric oxide and prostaglandin E2 . Nitric Oxide 197-209 interleukin 1 alpha Mus musculus 66-75 9797040-4 1998 Troglitazone also reduces interleukin-1alpha induced nitric oxide production in pancreatic beta-cells, which may be relevant in preventing nitric oxide mediated damage to these cells in the Type 1 diabetes process. Nitric Oxide 139-151 interleukin 1 alpha Mus musculus 26-44 9353295-1 1997 Treatment of mouse astrocyte cultures with combined interleukin (IL)-1alpha and tumor necrosis factor (TNF)-alpha induced expression of inducible nitric-oxide synthase (iNOS), resulting in sustained release of large amounts of nitric oxide, whereas TNF-alpha and IL-1alpha individually were unable to induce iNOS expression in astrocytes. Nitric Oxide 227-239 interleukin 1 alpha Mus musculus 52-75 7508126-2 1994 In vitro exposure of murine endothelial cells to various cytokines (interferon gamma, tumor necrosis factor alpha, and interleukin 1 alpha or 1 beta) resulted in their activation to kill schistosomula through an arginine-dependent mechanism involving production of nitric oxide (NO). Nitric Oxide 265-277 interleukin 1 alpha Mus musculus 119-148 9353295-1 1997 Treatment of mouse astrocyte cultures with combined interleukin (IL)-1alpha and tumor necrosis factor (TNF)-alpha induced expression of inducible nitric-oxide synthase (iNOS), resulting in sustained release of large amounts of nitric oxide, whereas TNF-alpha and IL-1alpha individually were unable to induce iNOS expression in astrocytes. Nitric Oxide 227-239 interleukin 1 alpha Mus musculus 263-272 9353295-4 1997 The p38(MAPK) pathway is specifically involved in TNF-alpha/IL-1alpha-induced iNOS expression, since iNOS protein and nitric oxide release in the presence of a specific inhibitor of p38(MAPK), 4-(4-fluorophenyl)-2-2-(4-hydroxyphenyl)-5-(4-pyridyl)-imidazole (FHPI), were dramatically diminished. Nitric Oxide 118-130 interleukin 1 alpha Mus musculus 60-69 33517187-5 2021 The results showed that XN has the capability to hinder the expression of nitric oxide synthase (INOS), IL-1beta-promoted inducible nitric oxide (NO), necrosis factor-alpha of tumor (TNF-alpha), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2) in vitro. Nitric Oxide 132-144 interleukin 1 alpha Mus musculus 104-112 34369548-8 2021 In vitro assays revealed that treatment with 18beta-GA considerably suppressed the expression of pro-inflammatory mediators and cytokines, including prostaglandin E2 (PGE2), tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and interleukin-6 (IL-6), which were induced by IL-1beta. Nitric Oxide 215-227 interleukin 1 alpha Mus musculus 348-356 34927076-4 2022 Treatment with IL-1beta and IFN-gamma stimulates expression of inducible nitric oxide synthase (iNOS) mRNA and antiviral and immune-associated genes as well as repression of islet identity factors in a subset of beta- and non-beta-endocrine cells in a nitric oxide-independent manner. Nitric Oxide 252-264 interleukin 1 alpha Mus musculus 15-23 35064430-9 2022 Treatment with crude extract (TSETOH) and fractions (TSHEX, TSTOL) significantly reduced (P < 0.001) the mRNA expression of pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha) and nitric oxide (NO) production in LPS-stimulated inflammation in RAW 264.7 cells in a dose-dependent manner. Nitric Oxide 183-195 interleukin 1 alpha Mus musculus 152-160 33878544-5 2021 In vitro cell experiments, the inflammatory response in chondrocytes is mediated via interleukin-1beta (IL-1beta), which led to abnormal secretion of pro-inflammatory factors, such as prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), cyclooxygenase-2 (COX-2), nitric oxide (NO) and inducible nitric oxide synthase (iNOS). Nitric Oxide 298-310 interleukin 1 alpha Mus musculus 104-112 33443518-9 2021 In vitro assays showed that the maltol pre-treatment significantly inhibited the expressions of multiple inflammatory factors induced by IL-1beta, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), nitric oxide (NO), interleukin-6 (IL-6) and tumor necrosis factor (TNF-alpha). Nitric Oxide 165-177 interleukin 1 alpha Mus musculus 137-145 32150895-6 2020 The present study showed that T. serrulatus venom induces the production of IL-1alpha and IL-1beta in the pancreas, which signal via IL-1R and provoke nitric oxide (NO) production as well as edema in beta-cells in islets. Nitric Oxide 151-163 interleukin 1 alpha Mus musculus 76-85 32150895-6 2020 The present study showed that T. serrulatus venom induces the production of IL-1alpha and IL-1beta in the pancreas, which signal via IL-1R and provoke nitric oxide (NO) production as well as edema in beta-cells in islets. Nitric Oxide 151-163 interleukin 1 alpha Mus musculus 90-98