Changes of protein expression profile in vascular tissues of spontaneously hypertensive rats treated by a compound Chinese herbal medicine

2011 ◽  
Vol 9 (6) ◽  
pp. 643-650 ◽  
Author(s):  
R Fan
2021 ◽  
Vol 22 (3) ◽  
pp. 1382
Author(s):  
Jelena Nesovic Ostojic ◽  
Milan Ivanov ◽  
Nevena Mihailovic-Stanojevic ◽  
Danijela Karanovic ◽  
Sanjin Kovacevic ◽  
...  

Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.


2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  

Abstract Objective A variety of circadian patterns of blood pressure after ischemic stroke in patients with essential hypertension appear to be a potential risk of stroke recurrence, but the mechanism is still unclear. This study intends to reveal the changes in blood pressure rhythm and circadian clock protein expression levels in spontaneously hypertensive rats (SHR) after ischemia-reperfusion, and the relationship between the two. Methods Using the SHR middle cerebral artery occlusion experimental model, the systolic blood pressure was continuously monitored for 24 hours after the operation to observe the blood pressure rhythm. The rat tail vein blood was taken every 3h, and the serum CLOCK, BMAL1, PER1 and CRY1 protein expression levels were detected by Elisa. Pearson correlation analysis counted the relationship between SHR blood pressure rhythm and circadian clock protein fluctuation after ischemia-reperfusion. Results The proportion of abnormal blood pressure patterns in the SHR + tMCAO group was significantly higher than that in the SHR group, the serum CLOCK expression was relatively constant, and the circadian rhythm of BMAL1, PER1 and CRY1 protein expression changed significantly. Pearson analysis showed that PER1 protein level was negatively correlated with dipper (r = -0.565, P = 0.002) and extreme-dipper (r = -0.531, P = 0.001) blood pressure, and was significantly positively correlated with non-dipper blood pressure (r = 0.620, P < 0.001). Conclusion The rhythm pattern of blood pressure after ischemia-reperfusion in SHR is obviously disordered, and it is closely related to the regulation of Per1 gene.


2021 ◽  
Vol 22 (21) ◽  
pp. 11812
Author(s):  
Atsunori Yamamoto ◽  
Kosuke Otani ◽  
Muneyoshi Okada ◽  
Hideyuki Yamawaki

Adipocytokine chemerin is a biologically active molecule secreted from adipose tissue. Chemerin elicits a variety of functions via chemokine-like receptor 1 (CMKLR1). The cardiovascular center in brain that regulates blood pressure (BP) is involved in pathophysiology of systemic hypertension. Thus, we explored the roles of brain chemerin/CMKLR1 on regulation of BP in spontaneously hypertensive rats (SHR). For this aim, we examined effects of intracerebroventricular (i.c.v.) injection of CMKLR1 small interfering (si)RNA on both systemic BP as measured by tail cuff system and protein expression in paraventricular nucleus (PVN) of SHR as determined by Western blotting. We also examined both central and peripheral protein expression of chemerin by Western blotting. Systolic BP of SHR but not normotensive Wistar Kyoto rats (WKY) was decreased by CMKLR1 siRNA. The decrease of BP by CMKLR1 siRNA persisted for 3 days. Protein expression of CMKLR1 in PVN of SHR tended to be increased compared with WKY, which was suppressed by CMKLR1 siRNA. Protein expression of chemerin in brain, peripheral plasma, and adipose tissue was not different between WKY and SHR. In summary, we for the first time revealed that the increased protein expression of CMKLR1 in PVN is at least partly responsible for systemic hypertension in SHR.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
L Urbano Pagan ◽  
M J Gomes ◽  
R L Damatto ◽  
M D M Cezar ◽  
D R A Reyes ◽  
...  

Abstract Introduction Physical exercise reduces systemic arterial blood pressure and improves cardiac remodeling. However, the effects of exercise during uncontrolled arterial hypertension remains poorly understood. This study evaluated the influence of physical training on cardiac remodeling in untreated spontaneously hypertensive rats (SHR). Methods Four experimental groups were used: sedentary (W-SED n=27) and trained (W-EX, n=31) normotensive Wistar rats, and sedentary (SHR-SED, n=27) and exercised (SHR-EX, n=32) hypertensive rats. At 13 months old, the exercise groups underwent treadmill exercise five days a week, for four months. Echocardiogram was performed to evaluate cardiac structures and function. In vitro myocardial function was analyzed in left ventricular (LV) papillary muscle preparations. Myocardial collagen was quantified by histology and hydroxyproline concentration and antioxidant enzyme activity was assessed by spectrophotometry. NADPH oxidase activity was analyzed by lucigenin reduction. Protein expression was quantified by Western blot. Matrix metalloproteinases (MMP) activity was evaluated by zymography. Statistical analyzes: two factor ANOVA and Bonferroni or Kruskal-Wallis and Dunn tests. Results Systolic blood pressure was higher in SHR groups. Exercised groups had greater physical capacity. Frequency of heart failure features was higher in hypertensive groups than controls; SHR-EX had a lower frequency of pleural effusion and tachypnea than SHR-SED. Echocardiogram showed lower LV wall thickness, LV relative wall thickness, left atrium diameter, and relaxation time in SHR-EX than SHR-SED. Myocardial function was better in SHR-EX (positive derivative of developed tension) than SHR-SED. SHR-EX had higher antioxidant enzyme activity than SHR-SED. Lipid hydroperoxide concentration, myocyte diameters, and phosphorylated JNK and total IkB protein expression were higher in hypertensive than control groups. Hydroxyproline, malondialdehyde, NADPH oxidase activity, and protein expression of collagen III, lysyl oxidase, TIMP-1, total JNK, phosphorylated p38, phosphorylated and total p65, and phosphorylated IkB did not differ between groups. Interstitial collagen fraction, MMP-2 activity, and protein expression of total p38, and total and phosphorylated ERK were higher in SHR-SED than W-SED. Exercise reduced MMP-2 activity and phosphorylated ERK in hypertensive rats. Conclusion Physical exercise improves physical capacity, reduces the frequency of heart failure features, and attenuates cardiac remodeling in spontaneously hypertensive rats. In addition, exercise increases antioxidant enzyme activity, decreases ERK phosphorylation and MMP-2 activity, and attenuates total ERK protein expression. Acknowledgement/Funding Fapesp, CNPq, Capes and UNESP


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