Data of the effects of acetone fraction from Sechium edule (Jacq.) S.w. edible roots in the kidney of endothelial dysfunction induced mice

Endothelial dysfunction induced by Angiotensin II (AG II) plays an important role in the pathogenesis of hypertension and is accompanied by a prooxidative condition, which in turn induces an inflammatory state, vascular remodeling, and tissue damage including the kidney (Schmitt and Dirsch, 2009) [1]. New drugs that can control several of these pathologies are required. Sechium edule has been reported to possess antioxidant, anti-inflammatory and antihypertensive activity (Ibarra-Alvarado et al., 2010) [2]. This paper contains data complementary to those published in Journal of Ethnopharmacology (Moreno et al., 2018) [3], evaluating the effect in kidney of hypertensive mice of the acetone fraction from S. edule to control de pro-oxidative state, reduction of the inflammatory adhesion molecule (ICAM) and recruitment of inflammatory cells.

paper contains data complementary to those published in Journal of Ethnopharmacology (Moreno et al., 2018) [3], evaluating the effect in kidney of hypertensive mice of the acetone fraction from S. edule to control de pro-oxidative state, reduction of the inflammatory adhesion molecule (ICAM) and recruitment of inflammatory cells.
& 2018 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Specifications Table
Subject area Medicine More specific subject area Use of extracts of Sechium edule to control endothelial dysfunction Type of data Text file and figures How data was acquired The Activity of antioxidant enzymes was measured by enzymatic reactions measuring the end product using a Spectrophotometer and analyzed in Excel and Microphotographs were acquired with a e Nikon ECLIPSE 80i microscope. The images were analyzed with the Metamorph software, v. 6.1.survey.

Data format Analyzed Experimental factors
The acetonic fraction of Sechium edule roots (rSe-ACE) were obtained and tested in its anti-oxidant, anti-inflammatory and anti-hypertensive capacity in a murine model of endothelial dysfunction [3].

Experimental features
Hypertension was induced in female mice by the chronic administration of angiotensin II for 10 weeks [1]. Treatments (Losartan or the acetonic fraction of Sechium edule) were coadministrated also for the 10 weeks. At the end of the experiment, kidneys were obtained and processed for biochemical or microscopic studies Data source location Sechium edule (Jacq.) Sw. roots were collected in the community of Tuxpanguillo, Veracruz, Mexico (18°47′00.5″N, 97°00′17.5″W, at 1721 m above mean sea level) in a period from April through May. Data accessibility Data is with this article.

Value of the data
A model of endothelial dysfunction is induced in rats by the chronic administration of angiotensin II. rSe-ACE is able to control Endothelial dysfunction (ED) and its associated pathologies. rSe-ACE is a good candidate for the development of a phytochemical medicine for ED.

Data
The dataset of this article provides information on the effects of the acetonic fraction of Sechium edule roots in the activity of antioxidant enzymes ( Fig. 1), in the expression of the inflammatory adhesion molecule ICAM 1 (Fig. 2) and in the recruitment of inflammatory cells on renal capsule ( Fig. 3) in kidney of endothelial dysfunction induced mice through the administration of Angiotensin [1].

Animals and experimental groups
Three groups of hypertensive female C57BL/6J mice, five mouse each, were coadministered with losartan (10 mg/kg) diluted in carboxymethylcellulose (CMC) 0.2% [4] or rSe-ACE (10 mg/kg) [2] diluted in water orally for 10 weeks. A fourth group was treated only with saline solution. Mice were regarded as hypertensive when blood pressure increased by 15% or more with respect to baseline blood pressure (systolic or diastolic). Mice were killed by CO 2 inhalation and exsanguinated at the end of the experiment

Tissue preparation for biochemical analysis
Kidneys were homogenized in ice-cold HEPES buffer (HEPES 25 mM, EDTA 1 mM, and phenylmethylsulfonyl fluoride [PMSF] 0.1 mM). Homogenates were centrifuged at 6000×g for 5 min at 4°C and supernatants were recovered. Protein concentration was determined by the Lowry method.   (Synergy HT, Biotek, Winooski, VT). Xanthine (0.1 mM) was used as a substrate for XO, and allopurinol (0.2 mM) was used as an inhibitor. Succinate (5 mM) was used as a substrate for mitochondrial O 2 − production, and antimycin (0.05 mM) was used to block the respiratory chain. L-arginine (L-Arg, 1 mM) was used as a substrate for NOS, while NG-nitro-L-arginine methyl ester (L-NAME, 1 mM) was used to block NOS activity. A blank without sample was run to subtract background fluorescence from each sample reading. Enzyme activity is expressed with respect to control readings.

Glutathione peroxidase assay
The activity of renal glutathione peroxidase (GPx) was assayed by measuring NADPH disappearance by optical density (OD) reading at 340 nm. GPx uses GSH to reduce tert-butyl hydroperoxide, thereby producing GSSG, which is readily reduced to GSH by GR using NADPH as a reducing equivalent donor. Blank reactions with the sample replaced by distilled water were subtracted from each assay reading. Data were expressed as units per mg protein.

Glutathione reductase assay
The activity of glutathione reductase (GR) was assayed using oxidized glutathione as a substrate. Briefly, GR reduces GSSG to GSH at the expense of NADPH; the disappearance of NADPH can be detected by reading OD at 340 nm.

Superoxide dismutase assay
The total activity of Superoxide Dismutase (SOD) was evaluated employing a competitive inhibition assay using a xanthine-XO system to reduce nitroblue tetrazolium (NBT). The percentage of NBT reduction in the sample-free control tube was 100%. The amount of protein that inhibited NBT reduction by 50% of the maximum reading was defined as one unit of SOD activity. Results were expressed as U/mg protein.

Histopathology and immunohistochemistry
After the last blood pressure measurement, mice were anesthetized with sodium pentobarbital (30 mg/kg i.p.) and perfused with ice-cold PBS (NaCl 140 mM, KCl 2 mM, and K 2 HPO 4 1.15 mM). Kidneys were removed. The organs were fixed in Zamboni solution (formaldehyde 2.0%, picric acid 0.2%, pH 7.0). Tissues were then dehydrated and embedded in paraffin. Tissue sections (5 μm) were transferred to poly-L-lysine-coated slides (Sigma) before being deparaffinized and rehydrated. For histopathological studies, the slides were stained with PAS stain. For Immunohistochemistry, kidney slides were deparaffined, rehydrated, and incubated with H 2 O 2 3%, albumin 5%, and Tween 20-PBS 1%. After treatment, tissue sections were incubated overnight with rat anti-mouse ICAM-1 (eBioscence) diluted 1:100 in albumin 0.1% and Tween 20-PBS 0.05%. After wash with PBS, tissues were incubated with 50 µl of biotinylated goat anti-rat IgG (MP Biomedicals) antibody, followed by HRP-labeled streptavidin solution (MP Biomedicals) at 37°C for 30 min, and developed with 3,3 diaminobenzidine (ZYMED, San Francisco, CA). The slides were counterstained with hematoxylin and photographed using a Nikon ECLIPSE 80i microscope. The images were analyzed with the Metamorph software, v. 6.1.

Transparency document. Supplementary material
Transparency document associated with this article can be found in the online version at http://dx. doi.org/10.1016/j.dib.2018.03.051.