Cardiac hypertrophy (CH) is a result of the physiological adaptation of the heart to coronary heart disease, hypertension, and other cardiovascular diseases. Sinomenine is extracted from Caulis Sinomenii . This study aimed to explore the specific mechanism of the action of sinomenine in cardiac hypertrophy (CH) via Nrf2/ARE signaling pathway in vivo and in vitro . To establish a model of CH, H9C2 cells were treated with angiotensin II (Ang II) and intraperitoneally injected with isoproterenol. Then the cells were treated with 50 and 100 μM sinomenine. TUNEL, HE, rhodamine-labeled phalloidin, and immunohistochemical staining were performed. Flow cytometry was used to measure apoptosis rates. mRNA expression of ANP, BNP, and β-MHC was determined by qRT-PCR. Furthermore, western blotting was performed to analyze protein expression. After sinomenine treatment, the surface area and apoptosis rates were decreased. Furthermore, the mRNA expression of ANP, BNP, and β-MHC, levels of reactive oxygen species and malondialdehyde, and protein expression of Caspase3 and Bax were down-regulated, and the protein expression of Bcl-2 was upregulated. Sinomenine activates the Nrf2/ARE signaling pathway, and inhibition of this signaling pathway reversed the effects of sinomenine. In animal experiments, sinomenine decreased the heart weight and left ventricular weight indices, as well as the expression of ANP, BNP, and β-MHC. Furthermore, sinomenine reduced the apoptosis rate and relieved CH-related oxidative stress by activating the Nrf2/ARE signaling pathway. Together, these findings reveal that sinomenine is a potential candidate drug for CH treatment and further research is required to generalize the result in human subjects.
Background: Endothelial dysfunction is common in patients undergoing hemodialysis (HD). However, little is known about the relationship between endothelial dysfunction and coenzyme Q10 (CoQ10) levels in HD patients. Methods: Eligible HD patients were enrolled in this study according to prespecified inclusion and exclusion criteria. Endothelial function was assessed by brachial artery flow-mediated dilation (FMD). Plasma CoQ10, serum malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) levels were measured. The potential confounders identified by univariate analyses (P < 0.15) were selected in a stepwise multiple regression model. Results: In total, 111 HD patients were enrolled in this study. The mean CoQ10 level was 633.53 ± 168.66 ng/mL, and endothelial dysfunction was prevalent (91.0%) using a cutoff value of 10% FMD. A significant correlation was observed between FMD and plasma CoQ10 level (r = 0.727, P < 0.001). After adjusting for potential parameters, a stepwise multivariate linear regression analysis revealed that CoQ10 level was an independent predictor of FMD (β = 0.018, P < 0.001). When CoQ10 was dichotomized using the median value (639.74 ng/mL), the conclusion remained unchanged (β = 0.584, P < 0.001). Pearson's correlation analyses revealed that plasma CoQ10 level was negatively correlated with MDA (r = −0.48, P < 0.001) and 8-OHdG (r = −0.43, P < 0.001) levels. Conclusion: Our data demonstrate that impaired brachial artery FMD was common in HD patients. CoQ10 level was independently associated with FMD, and oxidative stress may constitute a link between CoQ10 level and endothelial dysfunction in these patients. K E Y W O R D S coenzyme Q10, endothelial dysfunction, hemodialysis Patients with end-stage renal disease who undergo hemodialysis (HD) have a higher prevalence of atherosclerotic cardiovascular events than the general population. 1 Cardiovascular diseases, such as coronary artery disease, congestive heart failure and arrhythmias, represent the main causes of morbidity and mortality in patients undergoing HD. One study found that among dialysis patients, the pathological findings of heart disease included systolic dysfunction (15%), left ventricular hypertrophy (74%) and left ventricular dilation (36%). 2 In addition to traditional risk factors (such as hypertension, dyslipidemia and diabetes), endothelial dysfunction, hyperphosphatemia, vascular calcification, Jianjun Gao and Yongxing Xu contributed equally to this work.
This study aims to investigate the clinical significance of vector flow mapping (VFM) by observing and quantifying energy loss (EL) during different phases and in different left ventricle (LV) segments. Methods: 42 healthy physical examination subjects and 89 patients with hypertension (HTN) were enrolled in the present study. The patients with HTN were divided into two groups: the left ventricular hypertrophy group (LVH) (n = 51) and the non-left ventricular hypertrophy group (NLVH) (n = 38), while the healthy patients were control group. VFM analysis software DSA-RS1 was used to calculate EL during the rapid filling phase (P1), slow filling phase (P2), atrial contraction phase (P3), and rapid ejection phase (P4). The energy loss of basal segment (EL-B), middle segment (EL-M) and apical segment (EL-A) of left ventricle in different phases was calculated and compared among the three groups. Results: In controls, segmental EL showed a gradual increase from the apex to the base during diastole; however, the regularity was not found in the HTN patients. During both P1 and P2 EL-B, EL-M and EL-A were significantly higher in the NLVH group and the LVH group compared with the control group (P < 0.05). EL in LVH group was the highest among the three groups (P < 0.05). During P3, EL-B, EL-M and EL-A were increased in the NLVH group and LVH group compared with the control group. However, EL-M and EL-A in LVH group were significantly lower than the NLVH group (P < 0.05). During P4, EL of all segments was significantly higher in the NLVH group and LVH group compared with the control group (P < 0.05). Conclusion: VFM can visually quantify hydrodynamic LV changes in healthy subjects. The EL levels in the different LV segments during different phases were significantly higher in the patients with HTN compared with the healthy subjects.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.