scholarly journals Cholecystokinin Expression in the Development of Myocardial Hypertrophy

Scanning ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zhongshu Han ◽  
Sheng Bi ◽  
Yongsheng Xu ◽  
Xiaoying Dong ◽  
Lixia Mei ◽  
...  
Keyword(s):  
Myocardial Hypertrophy ◽  
Morphological Changes ◽  
Left Ventricular ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastrointestinal Hormone ◽  
Sham Operation ◽  
Aortic Constriction ◽  
Sham Operation Group ◽  
Protein Levels ◽  
Abdominal Aortic

Background. Expression of cholecystokinin is found in myocardial tissues as a gastrointestinal hormone and may be involved in cardiovascular regulation. However, it is unclear whether there is an increase in cholecystokinin expression in myocardial hypertrophy progression induced by abdominal aortic constriction. The study is aimed at exploring the relationship between cholecystokinin expression and myocardial hypertrophy. Methods. We randomly divided the 70 Sprague-Dawley rats into two groups: the sham operation group and the abdominal aortic constriction group. The hearts of rats were measured by echocardiography, and myocardial tissues and blood were collected at 4 weeks, 8 weeks, and 12 weeks after surgery. Morphological changes were assessed by microscopy. The cholecystokinin expression was evaluated by immunochemistry, Western blotting, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. Results. The relative protein levels of cholecystokinin were significantly increased in the abdominal aortic constriction groups compared with the corresponding sham operation groups at 8 weeks and 12 weeks. The cholecystokinin mRNA in the abdominal aortic constriction groups was significantly higher than the time-matched sham operation groups. Changes in the left ventricular wall thickness were positively correlated with the relative protein levels of cholecystokinin and the mRNA of cholecystokinin. Conclusions. The development of myocardial hypertrophy can affect the cholecystokinin expression of myocardial tissues.

scholarly journals QiShenYiQi Pill Improves Myocardial Hypertrophy Caused by Pressure Overload in Rats

2020 ◽  
Author(s):  
Shichao Lv ◽  
Qiang Wang ◽  
Meifang Wu ◽  
Meng Li ◽  
Xiaojing Wang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mechanism Of Action ◽  
Aortic Coarctation ◽  
Myocardial Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Control Group ◽  
Sham Operation ◽  
Tgf Beta ◽  
Abdominal Aortic

Abstract Background: QiShenYiQi pill (QSYQ), a traditional Chinese medicine, is widely used in the treatment of cardiovascular diseases, but its specific mechanism of action is still unclear. In the current study, we investigated the effect of QSYQ on myocardial hypertrophy in rats by partial abdominal aortic coarctation, and explored its mechanism of action.Methods: Wistar rats underwent the partial abdominal aortic coarctation were randomized into three groups: model, valsartan and QSYQ groups. And we treated rats which were sham operation as control group. Rats were euthanized at 4 and 8 weeks, and we weighed rat body mass, heart mass, and left ventricular mass. Myocardium sections were stained with hematoxylin and eosin (H&E) and Masson trichrome. Myocardial TGF- beta 1 and CTGF protein expression was detected by immunohistochemistry, and myocardial TGF-b1 and CTGF mRNA expression was detected by real-time qPCR. Results: QSYQ reduced HMI, LVMI and CVF, improved the changes of myocardial pathology, and reduced the degree of myocardial hypertrophy. After 4 weeks, QSYQ inhibited the mRNA and protein expression of TGF- beta 1 and CTGF. In addition, after 8 weeks, QSYQ reduced the positive area of TGF- beta 1 protein, and its effect is better than that of valsartan. Conclusions: QSYQ can effectively improve the degree of myocardial hypertrophy in the pressure overload rats, which is related to the mechanism of regulation of TGF- beta 1 and CTGF.

Mitochondrial adaptations during myocardial hypertrophy induced by abdominal aortic constriction

2014 ◽  
Vol 23 (5) ◽  
pp. 283-288 ◽  
Author(s):  
Zhusong Mei ◽  
Xinxing Wang ◽  
Weili Liu ◽  
Jingbo Gong ◽  
Xiujie Gao ◽  
...  
Keyword(s):  
Myocardial Hypertrophy ◽  
Aortic Constriction ◽  
Abdominal Aortic ◽  
Mitochondrial Adaptations

scholarly journals Antihypertrophic Memory after Regression of Exercise-induced Physiological Myocardial Hypertrophy is Mediated by the Long Noncoding RNA Mhrt779

Circulation ◽  
2021 ◽  
Author(s):  
Hairuo Lin ◽  
Yingqi Zhu ◽  
Cankun Zheng ◽  
Donghong Hu ◽  
Siyuan Ma ◽  
...  
Keyword(s):  
Western Blot ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Myocardial Hypertrophy ◽  
Quantitative Polymerase Chain Reaction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Sham Operation ◽  
Ventricular Ejection Fraction

Background: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5-6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress. Methods: C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning group, EHP) and sedentary mice (control group) then underwent transverse aortic constriction (TAC) or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated using echocardiography, invasive left ventricular hemodynamic measurement and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay (ChIP), and comprehensive identification of RNA-binding proteins by mass spectrometry (CHIRP-MS) and Western blot were used to investigate the role of Mhrt779 involved in the anti-hypertrophy effect induced by EHP. Results: At 1 and 4 weeks after TAC, the EHP group showed less increase in myocardial hypertrophy and lower expression of the Nppa and Myh7 genes than the sedentary group. At 4 weeks after TAC, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction (qPCR) revealed that the long noncoding myosin heavy chain associated RNA transcript Mhrt779 was one of the markedly upregulated long noncoding RNAs in the EHP group. Silencing of Mhrt779 attenuated the antihypertrophic effect of EHP in mice with TAC and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. By ChIP and qPCR, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of Mhrt779 . CHIRP-MS and Western blot showed that Mhrt779 can bind Brg1 to inhibit the activation of Hdac2/Akt/GSK3β pathway induced by pressure overload. Conclusions: Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of Mhrt779 /Brg1/Hdac2/p-Akt/p-GSK3β.

scholarly journals Leonurine Attenuates Pressure-Overload Cardiac Hypertrophy Induced By Abdominal Aortic Constriction In Rats

2021 ◽  
Author(s):  
Ding Xiaoli ◽  
Yuan Qingqing ◽  
Qian Haibing
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Ang Ii ◽  
Aortic Constriction ◽  
Qrt Pcr ◽  
Abdominal Aortic

Abstract Background: Myocardial hypertrophy occurs in many cardiovascular diseases. Leonurine (Leo) is commonly used for cardiovascular and cerebrovascular diseases. However, whether it can prevent cardiac hypertrophy is not known. The aim of this study was to investigate the effect and mechanism of Leonurine (Leo) against pressure-overload cardiac hypertrophy induced by abdominal aortic constriction (AAC) in rats. Methods: To answer this question, we prove it in the following way: Cardiac function was evaluated by hemodynamic; the left ventricle enlargement was measured by heart weight index (HWI) and left ventricular mass index (LVWI); myocardial tissue changes and myocardial cell diameter (MD) were determined by Hematoxylin and eosin (HE) staining; theβ-myosin heavy chain(β-MHC)and atrial natriuretic factor (ANF), which are recognized as a marker of cardiac hypertrophy, were determined by Real-time quantitative PCR (qRT-PCR), then another gene phospholipase C (PLC), inositol triphosphate (IP3), which associated with RAS were determined by Western blot(WB). angiotensin II (Ang II), angiotensin II type 1 receptor (AT1R) were determined by ELISA, WB and qRT-PCR methods. Finally, we measured the level of Ca2+ by microplate method and the protooncogene c-fos and c-myc mRNA in left ventricular myocardium by qRT-PCR.Results: Compare with control group, Leonurine can improve systolic dysfunction; inhibit the increase of left cardiac; inhibit myocardial cells were abnormally large and restrain the changes of cardiac histopathology; decrease the expression of β-MHC, ANF, Ang II, AT1R, c-fos and c-myc mRNA and the protein levels of PLC, IP3, AngII and AT1R in left ventricular myocardium, in addition, the content of Ca2+ also decrease. Conclusion: Therefore, Leonurine can inhibit cardiac hypertrophy induced by AAC and its effects may be associated with RAS.

Altered renal dopamine receptors during development of cardiac hypertrophy

1992 ◽  
Vol 262 (5) ◽  
pp. E569-E573
Author(s):  
P. K. Ganguly ◽  
K. Mukherjee ◽  
Y. Chen
Keyword(s):  
Cardiac Hypertrophy ◽  
Dopamine Receptors ◽  
Pressure Overload ◽  
Total Body Weight ◽  
Left Ventricular ◽  
Kidney Cortex ◽  
Sprague Dawley ◽  
Aortic Constriction ◽  
Compensatory Response ◽  
Abdominal Aortic

The characteristics of dopamine receptors were studied in heart and kidney using the radiolabeled receptor assay of [3H]spiperone during the development of cardiac hypertrophy. Male Sprague-Dawley rats (175-200 g) underwent abdominal aortic constriction above the renal arteries and were studied 3, 14, and 28 days thereafter. Sham-operated animals without aortic constriction were used as control. Although the ratio of left ventricular weight to total body weight was significantly increased 14 and 28 days after aortic constriction in animals, [3H]spiperone binding in left ventricular membrane was increased as early as 3 days after aortic constriction. At 14 days, the binding was still elevated and, by 28 days, it returned to control values. In contrast, membranes obtained from kidney cortex showed an elevation of [3H]spiperone binding only at 28 days after aortic constriction; at 3 days the binding values were decreased. A reciprocal correlation was found between the number of dopamine receptors and the activity of Na(+)-K(+)-ATPase at 28 days of aortic constriction; the enzyme activity, as measured by the release of 32Pi from [gamma-32P]ATP, was decreased in kidney cortex. Autoradiographic data also showed an increased number of dopamine receptors in kidney at 28 days after abdominal aortic constriction. These results suggest that the dopamine receptor is increased very early in heart in response to pressure overload as a result of a compensatory response to maintain an optimal left ventricular output. Kidney dopamine receptors are triggered at a later stage possibly to maintain fluid homeostasis secondary to the cardiac hypertrophic process.

scholarly journals The Effect of Biliary Decompression on Bacterial Translocation in Jaundiced Rats

HPB Surgery ◽  
1993 ◽  
Vol 7 (2) ◽  
pp. 99-110 ◽  
Author(s):  
Jin Wen Ding ◽  
Roland Andersson ◽  
Vasile Soltesz ◽  
Roger Willén ◽  
Steffen Loft ◽  
...  
Keyword(s):  
Liver Function ◽  
Obstructive Jaundice ◽  
Bacterial Translocation ◽  
Serum Alkaline Phosphatase ◽  
Morphological Changes ◽  
Sham Operation ◽  
Biliary Decompression ◽  
Septic Complications ◽  
Sham Operation Group ◽  
Duct Ligation

Patients with obstructive jaundice are prone to septic complications after biliary tract operations. Restoring bile flow to the intestine may help to decrease the complication rate. The present study is aimed at evaluating the effect of biliary decompression on bacterial translocation in jaundiced rats.Sixty-six male Sprague-Dawley rats were randomly allocated to six groups subjected to common bile duct ligation (CBDL) and transection (groups 2–6) or sham operation (group 1). In groups and 2 the incidence of enteric bacterial translocation was determined 2 weeks after sham operation or CBDL. In groups 3–6, biliary decompression was achieved by performing a choledochoduodenostomy after 2 weeks of biliary decompression. Bacterial translocation was then studied 1,2,3 and 5 weeks following biliary decompression.The rate of bacterial translocation to mesenteric lymph nodes in obstructive jaundice was significantly higher as compared with controls, and decreased with time to nil three weeks following biliary decompression. The incidence of bacterial translocation was closely correlated (r = 0.844; p = 0.034) with serum alkaline phosphatase activity and seemed to fit with the morphological changes noted in the small intestine. The decrease in bacterial translocation, however, lags behind the recovery of liver function as measured by routine liver function tests and antipyrine clearance.Obstructive jaundice thus promotes bacterial translocation in the rat. Biliary decompression gradually decreases the rate of bacterial translocation.

Tongsaimai reverses the hypertension and left ventricular remolding caused by abdominal aortic constriction in rats

2020 ◽  
Vol 246 ◽  
pp. 112154 ◽  
Author(s):  
Qinghai Meng ◽  
Yao Guo ◽  
Dini Zhang ◽  
Qichun Zhang ◽  
Yu Li ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Aortic Constriction ◽  
Abdominal Aortic

scholarly journals Impacts of a Specific Cyclooxygenase-2 Inhibitor on Pressure Overload–Induced Myocardial Hypertrophy in Rats

2019 ◽  
Vol 22 (6) ◽  
pp. E432-E437
Author(s):  
Zhixiang Xie ◽  
Shuyin Wang ◽  
Zijing Liang ◽  
Liangbo Zeng ◽  
Rongde Lai ◽  
...  
Keyword(s):  
Myocardial Hypertrophy ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cyclooxygenase 2 ◽  
Inflammatory Factors ◽  
Heart Weight ◽  
Sham Operation ◽  
Surgery Group ◽  
Tnf Α

Objective: The aim of this study was to observe the impacts of the specific cyclooxygenase-2 inhibitor celecoxib on cardiac structures, functions, and inflammatory factors during the process of pressure overload–induced myocardial hypertrophy. Methods: Twenty-four male Sprague Dawley rats were randomly divided into 3 groups: the sham operation group, the surgery group, and the celecoxib group. The model was established according to the abdominal aortic coarctation method. Results: At 16 weeks, rats in the celecoxib group were fed a celecoxib-mixed diet (10 mg/kg) for 8 consecutive weeks. At week 24 after model establishment, the cardiac structures and functions were observed; changes in the levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, prostaglandin E2 (PGE2), C-reactive protein (CRP), and uric acid (UA) were detected; and the contents of Smad1/2/3 proteins (Smad1, Smad2, and Smad3)  were determined. Left ventricular mass index, the heart weight/body weight ratio, and TNF-α, TGF-β, PGE2, CRP, and UA levels of the celecoxib group were all significantly decreased relative to those of the surgery group (P < .05); moreover, the cardiac functions were significantly improved compared to those of the surgery group (P < .05). Conclusions: These results show that inflammatory factors are involved in the myocardial hypertrophy process and that celecoxib may reverse myocardial hypertrophy through a variety of pathways.

scholarly journals Luhong Formula Has a Cardioprotective Effect on Left Ventricular Remodeling in Pressure-Overloaded Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Qian Liu ◽  
Hui-Yan Qu ◽  
Hua Zhou ◽  
Jing-Feng Rong ◽  
Tian-Shu Yang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Caspase 3 ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Sham Operation ◽  
Model Group ◽  
Enos Expression ◽  
Sham Operation Group ◽  
Operation Group

Background. Luhong formula (LHF)—a traditional Chinese medicine containing Cervus nippon Temminck, Carthamus tinctorius L., Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao, Codonopsis pilosula (Franch.) Nannf., Cinnamomum cassia Presl, and Lepidium apetalum Willd—is used in the treatment of heart failure, but little is known about its mechanism of action. We have investigated the effects of LHF on antifibrosis. Methods. Forty-eight SD male rats were randomly assigned into six groups (n = 8), model group, sham-operation group, perindopril group (0.036 mg/ml), LHF high doses (LHF-H, 1.44 g/mL), LHF middle doses (LHF-M, 0.72 g/mL), and LHF low doses (LHF-L, 0.36 g/mL). Except the sham-operation group, the other groups were received an abdominal aorta constriction to establish a model of myocardial hypertrophy. The HW and LVW were measured to calculate the LVW/BW and HW/BW. ELISA was used to detect the serum concentration of BNP. The expressions of eNOS, TGF-β1, caspase-3, VEGF, and VEGFR2 in heart tissues were assessed by western blot analysis. mRNA expressions of eNOS, Col1a1, Col3a1, TGF-β1, VEGF, and VEGFR2 in heart tissues were measured by RT-PCR. The specimens were stained with hematoxylin-eosin (HE) and picrosirius red staining for observing the morphological characteristics and collagen fibers I and III of the myocardium under a light microscope. Results. LHF significantly lowered the rat’s HW/BW and LVM/BW, and the level of BNP in the LHF-treated group compared with the model group. Histopathological and pathomorphological changes of collagen fibers I and III showed that LHF inhibited myocardial fibrosis in heart failure rats. Treatment with LHF upregulated eNOS expression in heart tissue and downregulated Col1a1, Col3a1, TGF-β1, caspase-3, VEGF, and VEGFR2 expression. Conclusion. LHF can improve left ventricular remodeling in a pressure-overloaded heart failure rat model; this cardiac protective ability may be due to cardiac fibrosis and attenuated apoptosis. Upregulated eNOS expression and downregulated Col1a1, Col3a1, TGF-β1, caspase-3, VEGF, and VEGFR2 expression may play a role in the observed LHF cardioprotective effect.

Effect of a mild exercise program on myocardial function and the development of hypertrophy

1979 ◽  
Vol 46 (2) ◽  
pp. 354-360 ◽  
Author(s):  
A. F. Cutilletta ◽  
K. Edmiston ◽  
R. T. Dowell
Keyword(s):  
Cardiac Index ◽  
Myocardial Function ◽  
Myocardial Hypertrophy ◽  
Exercise Program ◽  
Pressure Overload ◽  
Ascending Aorta ◽  
Sham Operation ◽  
Aortic Constriction ◽  
Sedentary Animal ◽  
Slight Elevation

Cardiac function and the development of myocardial hypertrophy were studied in rats conditioned by an exercise program consisting of 8 wk of running on a treadmill. At the end of the training period a group of exercised and sedentary rats was subjected to hemodynamic evaluation under general anesthesia. Except for a slight elevation in the heart rates of the exercised animals there were no significant differences between the exercised and sedentary rats at rest. Following an increase in afterload or a period of hypoxia, the cardiac index of the exercised animals remained significantly higher than that of the sedentary controls. These differences were related to changes in stroke volume. Another group of exercised and sedentary animals underwent either constriction of the ascending aorta or a sham operation. Sedentary rats developed significant hypertrophy at 3 days but had no hypertrophy at 1 day after aortic constriction. Exercised rats, however, developed significant myocardial hypertrophy by 1 day after pressure overload. These data suggest that the heart from an exercised animal is better able to tolerate increases in afterload and hypoxia and can respond with compensatory myocardial hypertrophy more rapidly than the heart of a sedentary animal.

Sign in / Sign up

Export Citation Format

Share Document