Journal: International journal of molecular sciences

Article Title: Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress.

doi: 10.3390/ijms241310839

Figure Lengend Snippet: Figure 1. Effect of administration of uric acid on the release of Ang II from RBL-2H3 cells. (A,B): The viability of RBL-2H3 cells was determined via CCK-8 assay after treatment with various uric acid concentrations for 24 h or 48 h. (C): Toluidine blue staining of RBL-2H3 after treatment with various uric acid concentrations for 24 h or 48 h. Scale bar = 50 µm. (D,E): Ang II levels in each group after treatment with various uric acid concentrations for 24 h or 48 h. Results are shown as mean ± S.D. (n = 4). * p < 0.05, ** p < 0.01 indicate statistically significant differences compared with the control group.

Article Snippet: MedChemExpress (Monmouth Junction, NJ, USA) supplied Angiotensin II human.

Techniques: CCK-8 Assay, Staining, Control

Journal: International journal of molecular sciences

Article Title: Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress.

doi: 10.3390/ijms241310839

Figure Lengend Snippet: Figure 8. Effects of SCG or VAL on renal oxidative stress in hyperuricemic rats. (A–D): Renal GSH level, renal GSH-Px activity, renal GR activity, and renal MDA level in each group. (E): Serum Ang II level in each group. (F,G): The viability of HK-2 cells was determined via CCK-8 assay after treatment with various Ang II concentrations for 24 h or 48 h. (H): Reactive oxygen species (ROS) levels in each group after incubation of HK-2 cells with different concentrations of Ang II for 24 or 48 h (100×). Results are shown as mean ± S.D. (n = 6). * p < 0.05, ** p < 0.01 indicate statistically significant differences compared with the control group. # p < 0.05, ## p < 0.01 indicate statistically significant differences compared with the model group.

Article Snippet: MedChemExpress (Monmouth Junction, NJ, USA) supplied Angiotensin II human.

Techniques: Activity Assay, CCK-8 Assay, Incubation, Control

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: A- Mice survival after hypertension onset (days after beginning of Ang II infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques:

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: A- In vivo imaging (microm) performed on 129Sv (129) and C57BL6/J (B6J) mice 8 days after angiotensin-2 pump implantation shows haemorrhage (arrows) and hard exudates (asterisks). Haemorrhagic spots are only found on the 129Sv eye fundus and density of hard exudates is increased in 129 mice compared to B6J mice. B-Haemorrhagic spots (arrow heads) in retinas at day 7 of hypertensive challenge and associated quantification. Values represent mean ± SEM of 5 mice per group. * p < 0.05. C- Subretinal swelling assessed by OCT at day 7 of hypertensive challenge and associated quantification. The white arrow shows retinal detachment. D- Retinal capillary density assessed at day 7 of hypertensive challenge. Representative images of the retina vascular network stained with lectin antibody. Values represent mean ± SEM of 4 B6J mice and 8 129 mice. *** p < 0.001.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques: In Vivo Imaging, Staining

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: Typical ECG changes seen in SV129 mice treated for 2 weeks with angiotensin II (n = 5-7 mice/group. A. episode of atrial flutter B. atrial fibrillation. C. ventricular ectopy seen in the Ang II group; D. short run of ventricular tachycardia; E. sustained ventricular tachycardia degenerating in ventricular fibrillation and cardiac death.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques:

Journal: Molecular & Cellular Proteomics : MCP

Article Title: Region- and Cell-type–Resolved Multiomic Atlas of the Heart

doi: 10.1016/j.mcpro.2025.100922

Figure Lengend Snippet: The protective role of atRA in heart failure. A , α-Actinin staining was performed to identify NRCMs. Representative images and quantification of cell size of total 30 microscope fields in each group (group1: NRCMs, group2: NRCMs treated with atRA, group3: NRCM stimulated with Ang II, and group4: NRCM stimulated with Ang II then treated with atRA) are shown. B , the boxplot shows the myocyte cross-sectional area in the four groups. The mRNA levels of hypertrophic genes ( Anp, Bnp ) were determined using qRT-PCR. n = 4 biological replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. C , the cluster heatmaps indicate the expression patterns of two cluster of proteins detected in NRCM under different conditions (Ang II nonstimulate, Ang II stimulated, Ang II stimulated with atRA treatment). The color bar indicates normalized z-scored iBAQ. The top GOBP terms enriched by each cluster are shown on the right . D , representative global heart photographs of four mice are shown (scale bar represents 2 mm). E , the bar plot shows the heart weight/tibia, heart rate, LV ejection fraction, fractional shortening, LV internal dimension at end-diastole, LV internal dimension at end-systole, LV anterior wall thickness at end-diastole, LV posterior wall thickness at end-systole, all measurements are shown as mean ± SEM. n = 7 biological replicates in Sham group and n = 8 biological replicates in TAC group. F , Masson staining showed strong fibrosis in ventricular regions. Scale bars represent 100 μm. G , the mRNA levels of Ctgf, Cola1 , and Col3a1 were determined using qRT-PCR. n = 6 biologically replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. H , hematoxylin-eosin (H&E, scale bar = 1 mm) staining and wheat germ agglutinin (WGA, scale bar = 30 μm) staining were performed to determine the hypertrophic degree of the hearts. I , the boxplot shows the myocyte cross-sectional area in the four groups. The mRNA levels of hypertrophic genes ( Anp, Bnp ) were determined using qRT-PCR. n = 6 biologically replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. J , the bar plot indicates the GOBP enriched in the proteins upregulated in TAC group ( orange ) and downregulated in TAC group ( green ), compared with sham oil group. K , the bar plot shows the GOBP enriched by the proteins upregulated in TAC mice treated with atRA ( orange ) and downregulated in TAC mice treated with atRA ( green ), compared with TAC oil group. L , the western blots show the expression patterns of Rxra, Rxrb, and Gapdh in the four groups (group1: WT mice treated with corn oil, group2: TAC mice treated with corn oil, group3: WT mice treated with atRA, Group4: TAC mice treated with atRA). M , The mRNA level of Rxra and Rxrb were determined using qRT-PCR. n = 7 biologically replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. N , the hypothetical mechanism of atRA rescuing heart from cardiac hypertrophy. Under physiological conditions, retinol is oxidized to retinaldehyde by either alcohol dehydrogenase or retinol dehydrogenase (RDH), and retinaldehyde is oxidized to RA by aldehyde dehydrogenase (ALDH). RA is then released and taken up by cardiomyocytes and cellular-RA–binding protein (CRABP) facilitates RA to transport to the nucleus where RA can bind the RA receptor (RAR). When mouse is treated with atRA (60 mg/kg/day) for 4 weeks after TAC surgery, cardiac hypertrophy is relieved. The atRA may act through the activation of Rxr family and maintains cardiac function.

Article Snippet: NRCMs were isolated from 1 to 3 days old Sprague-Dawley rats and cultured in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 (DMEM/F12) (Invitrogen, 11330032) with 10% fetal bovine serum for 24 h. Then medium was changed into serum-free DMEM/F12 for 24 h. One micromolar of Angiotensin II (MCE, HY- 13948) treated cells individually or treated cells with 1 μM atRA (Sigma, R2625) collectively for 24 h. After 24 h incubation, cardiomyocytes were collected and lysed for further quantitative real-time PCR (qRT-PCR).

Techniques: Staining, Microscopy, Quantitative RT-PCR, Expressing, Western Blot, Binding Assay, Activation Assay

Journal: Experimental and Therapeutic Medicine

Article Title: Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

doi: 10.3892/etm.2017.5198

Figure Lengend Snippet: Effects of Rb1 and Rg3 on blood pressure, CWI and RAS activity in the serum. (A) SBP, (B) DBP and (C) PP of rats prior to and following 6 weeks treatment. (D) Body and (E) heart weights and (F) CWI. Serum (G) ACE and (H) Ang II levels. Data are presented as the mean ± standard deviation, n=8 (A-F) or n=6 (G-H) for each group. *P<0.05 vs. WKY group prior to treatment; # P<0.05 vs. WKY group following treatment; $ P<0.05 vs. SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; CWI, cardiac weight index; RAS, renin angiotensin system; SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; ACE, angiotensin converting enzyme; Ang II, angiotensin II; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Article Snippet: ACE (CSB-E04490r) and Ang II (CSB-E04494r) ELISA kits were purchased from Cusabio Biotech Co., Ltd. (Wuhan, China) and the assays were completed by this company.

Techniques: Activity Assay, Standard Deviation

Journal: Experimental and Therapeutic Medicine

Article Title: Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

doi: 10.3892/etm.2017.5198

Figure Lengend Snippet: Effects of Rb1 and Rg3 on RAS and TGF-β1 levels in the myocardium. (A) Representative IHC staining photomicrographs of myocardium tissue. (Magnification, ×400). Antibodies against ACE, Ang II, AT1 and TGF-β1 were used as the primary antibodies. (B-E) Quantitative results of IHC staining, which were presented as IOD/Area and were proportional to the levels of ACE, Ang II, AT1 and TGF-β1. Data are presented as the mean ± standard deviation, n=4. # P<0.05 vs. the WKY group following treatment; $ P<0.05 vs. the SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; RAS, renin angiotensin system; TGF-β1, transforming growth factor β1; IHC, immunohistochemistry; ACE, angiotensin converting enzyme; Ang II, angiotensin II; AT1, Ang II receptor type 1; IOD, integrated optical density; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Article Snippet: ACE (CSB-E04490r) and Ang II (CSB-E04494r) ELISA kits were purchased from Cusabio Biotech Co., Ltd. (Wuhan, China) and the assays were completed by this company.

Techniques: Immunohistochemistry, Standard Deviation

Journal: Scientific Reports

Article Title: Sniffer cells for the detection of neural Angiotensin II in vitro

doi: 10.1038/s41598-019-45262-4

Figure Lengend Snippet: ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG III induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.

Article Snippet: Carbachol (50 μM), Angiotensin 1–7 (0.1–100 nM), Bradykinin (0.1–100 nM), and Losartan (10 μM) were purchased from Tocris (Minneapolis, MN) and Angiotensin III (0.1–100 nM) was purchased from Alomone Labs (Jerusalem, Israel).

Techniques: Fluorescence, Control, Transfection