PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20646585-8 2010 And the early L-NAME subgroup in apoE(-/-) mice was the most remarkable (P < 0.05). NG-Nitroarginine Methyl Ester 14-20 apolipoprotein E Mus musculus 33-37 22040569-8 2011 RESULTS: In WT and apoE-/- mice, SBP and urinary protein increased following L-NAME injection. NG-Nitroarginine Methyl Ester 77-83 apolipoprotein E Mus musculus 19-23 22040569-9 2011 Fetal and placental weights and NO concentrations were reduced and total cholesterol, triglycerides and free fatty acid levels were increased in early and mid L-NAME groups in WT and apoE-/- mice, compared with the NS group. NG-Nitroarginine Methyl Ester 159-165 apolipoprotein E Mus musculus 183-187 22040569-11 2011 RT-PCR and Western blotting analysis showed that the mRNA and protein levels of LCHAD expression were significantly down-regulated in the early and mid L-NAME groups but not in the late L-NAME group in the WT and apoE-/- mice compared with the corresponding NS groups. NG-Nitroarginine Methyl Ester 152-158 apolipoprotein E Mus musculus 213-217 22321750-9 2011 RESULTS: The expressions of mRNA and protein of LCHAD significantly decreased in early and middle L-NAME groups in both apoE(-/-) and WT mice (P < 0.05). NG-Nitroarginine Methyl Ester 98-104 apolipoprotein E Mus musculus 120-124 22321750-11 2011 The changes were marked in the early HF + L-NAME subgroup in apoE(-/-) mice (P < 0.05). NG-Nitroarginine Methyl Ester 42-48 apolipoprotein E Mus musculus 61-65 22321750-12 2011 As compared with other groups, the placental expressions of mRNA and protein of p47phox and COX-2 markedly increased in the early and middle L-NAME subgroups in apoE(-/-) mice (P < 0.05), especially in early and middle HF + L-NAME subgroups in apoE(-/-) mice (P < 0.05). NG-Nitroarginine Methyl Ester 141-147 apolipoprotein E Mus musculus 161-165 22321750-20 2011 In early and middle L-NAME groups, oxidative stress and inflammatory injury occur in both apoE(-/-) and WT mice. NG-Nitroarginine Methyl Ester 20-26 apolipoprotein E Mus musculus 90-94 20646585-11 2010 The plasma lipid levels of apoE(-/-) HF + L-NAME group were the highest among all the groups (P < 0.05). NG-Nitroarginine Methyl Ester 42-48 apolipoprotein E Mus musculus 27-31 20646585-12 2010 Fetal and placental weights significantly decreased in early and middle L-NAME groups in both apoE(-/-) and WT mice (P < 0.05). NG-Nitroarginine Methyl Ester 72-78 apolipoprotein E Mus musculus 94-98 20646585-15 2010 The fetal and placental weights in HF groups were lower than SC groups and the changes in early HF + L-NAME subgroup in apoE(-/-) mice were the most remarkable (P < 0.05). NG-Nitroarginine Methyl Ester 101-107 apolipoprotein E Mus musculus 120-124 20646585-18 2010 High-fat dietary may aggravate the impact of L-NAME pre-eclampsia on pregnancy outcomes at an early gestational stage especially in ApoE(-/-) mice. NG-Nitroarginine Methyl Ester 45-51 apolipoprotein E Mus musculus 132-136 32301289-4 2020 Yet, those protective effects are abrogated by using NOS inhibitor L-NAME in Apoe- / - mice received DMY. NG-Nitroarginine Methyl Ester 67-73 apolipoprotein E Mus musculus 77-81 20167907-8 2010 Moreover, the magnitude of L-NAME-induced contractions of isolated middle cerebral arteries from ApoE(-/-) mice was <50% of that in WT mice (P<0.05), whereas in Nox2(-/-)/ApoE(-/-) mice, the contractile response was comparable to WT responses. NG-Nitroarginine Methyl Ester 27-33 apolipoprotein E Mus musculus 97-101 20167907-8 2010 Moreover, the magnitude of L-NAME-induced contractions of isolated middle cerebral arteries from ApoE(-/-) mice was <50% of that in WT mice (P<0.05), whereas in Nox2(-/-)/ApoE(-/-) mice, the contractile response was comparable to WT responses. NG-Nitroarginine Methyl Ester 27-33 apolipoprotein E Mus musculus 177-181 15639308-5 2005 Inhibition of nitric oxide (NO) synthesis with N(omega)-nitro-L-arginine methyl ester (L-NAME) significantly inhibited NO-mediated vascular responses and accelerated atherosclerosis in apoE-KO mice, supporting a protective role of NO against atherosclerosis. NG-Nitroarginine Methyl Ester 47-85 apolipoprotein E Mus musculus 185-189 15639308-5 2005 Inhibition of nitric oxide (NO) synthesis with N(omega)-nitro-L-arginine methyl ester (L-NAME) significantly inhibited NO-mediated vascular responses and accelerated atherosclerosis in apoE-KO mice, supporting a protective role of NO against atherosclerosis. NG-Nitroarginine Methyl Ester 87-93 apolipoprotein E Mus musculus 185-189 11692031-9 2001 Treatment of arteries with NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester inhibited relaxations to acetylcholine to the same extent in apoE-deficient mice as in control mice. NG-Nitroarginine Methyl Ester 49-87 apolipoprotein E Mus musculus 149-153 10775149-3 2000 L-NAME treatment resulted in a significant inhibition of NO-mediated vascular responses and a significant increase in the atherosclerotic plaque/surface area in the aorta of apoE-KO mice. NG-Nitroarginine Methyl Ester 0-6 apolipoprotein E Mus musculus 174-178 16516241-9 2006 L-NAME significantly inhibited LDL oxidation by smooth muscle cells from iNOS(+/+)/apoE(-/-) mice (P=0.048), but it had no effect on LDL oxidation by cells from iNOS(-/-)/apoE(-/-) mice. NG-Nitroarginine Methyl Ester 0-6 apolipoprotein E Mus musculus 83-87 29784903-7 2018 L-NAME, tunicamycin, and Genipin attenuated vasodilation in WT, WT-EX and ApoE KO-EX, but not in ApoE KO. NG-Nitroarginine Methyl Ester 0-6 apolipoprotein E Mus musculus 74-78 29707746-9 2019 L-NAME reduced vasodilator responses to acetylcholine; this effect was lower in ApoE-/- cadmium-treated mice, suggesting reduction in nitric oxide (NO) bioavailability. NG-Nitroarginine Methyl Ester 0-6 apolipoprotein E Mus musculus 80-84 30773021-7 2019 SAHH+/- mice or apoE-/- mice with SAHH inhibition showed impaired endothelium-dependent vascular relaxation and decreased nitric oxide bioavailability after treatment with acetylcholine; this was completely abolished by the administration of the endothelial nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester. NG-Nitroarginine Methyl Ester 290-322 apolipoprotein E Mus musculus 16-20 26201383-7 2015 L-NAME (NOS inhibitor) reduced baseline flow and RH to a lesser extent in ApoE KO (by ~19% and 31%) vs. WT (~30% and 59%, respectively), and abolished the sex difference in RH. NG-Nitroarginine Methyl Ester 0-6 apolipoprotein E Mus musculus 74-78 24587793-6 2014 L-NAME also caused a doubling of aortic renin and angiotensinogen mRNA level in the ApoE-null mice but not in the DKO, and it upregulated eNOS in the DKO mice only. NG-Nitroarginine Methyl Ester 0-6 apolipoprotein E Mus musculus 84-88 24587793-7 2014 These data suggest that, in the ApoE-null mouse, PPAR alpha contributes to the proatherogenic effect of unopposed RAS/AII action induced by L-NAME, an effect which is associated with Nox1 and iNOS induction, and is independent of blood pressure and serum lipids. NG-Nitroarginine Methyl Ester 140-146 apolipoprotein E Mus musculus 32-36 23736171-5 2015 The vascular cell adhesion molecule-1 expression levels and degree of monocyte/macrophage accumulation in the intima were also considerably reduced in AT2-Tg/apoE(-/-) mice; these phenomena were completely reversed by L-NAME treatment. NG-Nitroarginine Methyl Ester 218-224 apolipoprotein E Mus musculus 158-162 23044319-8 2012 RESULTS: In WT and apoE(-/-) L-NAME subgroups, blood pressure and urine protein were significantly higher than those in all the gestational age matched NS groups (P < 0.05). NG-Nitroarginine Methyl Ester 29-35 apolipoprotein E Mus musculus 19-23 23044319-9 2012 Compared to other groups, remarkable liver fatty infiltration and lipid storage in placenta were found in early- and mid-L-NAME subgroups in apoE(-/-) mice (P < 0.05), especially in the early- and mid-HF+L-NAME subgroups in apoE(-/-) mice (P < 0.05). NG-Nitroarginine Methyl Ester 121-127 apolipoprotein E Mus musculus 141-145 23044319-11 2012 Morphology histopathologic examination of placentas showed varying degrees of fibrinoid necrosis and villous interstitial edema in early- and mid-L-NAME both in HF and SC of apoE(-/-) and WT subgroups compared to NS controls (P < 0.05). NG-Nitroarginine Methyl Ester 146-152 apolipoprotein E Mus musculus 174-178