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1.
Fig. 6.

Fig. 6. From: Soluble epoxide hydrolase gene deletion attenuates renal injury and inflammation with DOCA-salt hypertension.

Renal NF-κB activity and urinary MCP-1 excretion between DOCA-salt hypertension groups. A: renal NF-κB activity increased in the WT DOCA-salt (n = 6/group, *P < 0.05 vs. WT control) and was significantly reduced in Ephx2−/− DOCA-salt mice (n = 6/group, +P < 0.05 vs. WT DOCA-salt). B: urinary MCP-1 excretion in Ephx2−/− DOCA-salt as well as in WT DOCA-salt plus tAUCB was significantly reduced compared with WT DOCA-salt (n = 6/group, P < 0.05).

Marlina Manhiani, et al. Am J Physiol Renal Physiol. 2009 September;297(3):F740-F748.
2.
Fig. 3.

Fig. 3. From: Soluble epoxide hydrolase gene deletion attenuates renal injury and inflammation with DOCA-salt hypertension.

Glomerular nephrin immunofluorescence (A) and levels of relative fluorescent intensity (B) between DOCA-salt groups (n = 6/group). Glomerular nephrin fluorescent intensity decreased significantly in WT DOCA-salt (*P < 0.05 vs. WT control), while no change was seen in Ephx2−/− DOCA-salt mice (+P < 0.05 vs. Ephx2−/− control). Intensity in the WT DOCA-salt plus tAUCB increased significantly compared with WT DOCA-salt mice (+P < 0.05).

Marlina Manhiani, et al. Am J Physiol Renal Physiol. 2009 September;297(3):F740-F748.
3.
Fig. 4.

Fig. 4. From: Soluble epoxide hydrolase gene deletion attenuates renal injury and inflammation with DOCA-salt hypertension.

Glomerular desmin expression in DOCA-salt hypertension groups. Glomerular desmin immunofluorescence (A) and levels of relative fluorescent intensity (B) between DOCA-salt groups (n = 6/group) are shown. Glomerular desmin fluorescent intensity increased significantly in WT DOCA-salt compared with WT control group (*P < 0.05), while no change was noted between Ephx2−/− DOCA-salt and control groups.

Marlina Manhiani, et al. Am J Physiol Renal Physiol. 2009 September;297(3):F740-F748.
4.
Fig. 5.

Fig. 5. From: Soluble epoxide hydrolase gene deletion attenuates renal injury and inflammation with DOCA-salt hypertension.

Renal inflammatory gene expression between DOCA-salt hypertension groups. Gene expression between WT and Ephx2−/− control groups (A) and gene expression between WT control and WT DOCA-salt groups (B) are shown. Gene expression between Ephx2−/− control and Ephx2−/− DOCA-salt groups (C) and gene expression between WT and Ephx2−/− DOCA-salt groups (D) are also shown. mRNA expression of proinflammatory cytokines increased within WT as well as Ephx2−/− DOCA-salt compared with control groups, while Ephx2−/− DOCA-salt expression of inflammatory genes was less than WT DOCA-salt mice.

Marlina Manhiani, et al. Am J Physiol Renal Physiol. 2009 September;297(3):F740-F748.
5.
Fig. 2.

Fig. 2. From: Soluble epoxide hydrolase gene deletion attenuates renal injury and inflammation with DOCA-salt hypertension.

Renal injury in DOCA-salt hypertension groups. Albuminuria increased significantly in WT DOCA-salt compared with WT control (n = 6/group; A). Ephx2−/− DOCA-salt as well as WT DOCA-salt plus tAUCB mice displayed less albuminuria compared with WT DOCA-salt mice (+P < 0.05; A). B: Masson's trichrome staining in kidney histological sections. C: Masson's trichrome score (n = 6/group). Collagen deposition as assessed by the intensity of Masson's trichrome stain was increased in WT DOCA-salt compared with control mice (*P < 0.05). Masson's trichrome score was reduced in Ephx2−/− DOCA-salt compared with WT DOCA-salt (+P < 0.05).

Marlina Manhiani, et al. Am J Physiol Renal Physiol. 2009 September;297(3):F740-F748.
6.
Fig. 1.

Fig. 1. From: Soluble epoxide hydrolase gene deletion attenuates renal injury and inflammation with DOCA-salt hypertension.

Mean arterial pressure (MAP) increased significantly in both wild-type (WT) and Ephx2−/− DOCA-salt groups compared with their respective controls (n = 6/group *P < 0.05; A). MAP in the Ephx2−/− DOCA-salt group was significantly lower than WT DOCA-salt. MAP measurements were also made in WT and Ephx2−/− DOCA-salt groups treated with the soluble epoxide hydrolase (sEH) inhibitor tAUCB (n = 6/group; B). MAP was be significantly lower in WT and Ephx2−/− DOCA-salt+tAUCB groups compared with WT DOCA-salt, and there is no difference in MAP between Ephx2−/− and WT DOCA-salt tAUCB-treated groups. sEH protein expression was absent from the Ephx2−/− mice (C), and Cyp2c44 expression remained unchanged in both WT and Epx2−/− kidney homogenates (D).

Marlina Manhiani, et al. Am J Physiol Renal Physiol. 2009 September;297(3):F740-F748.

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