Delayed neutrophil apoptosis mediates intermittent hypoxia-induced progressive heart failure in pressure-overloaded rats

Li, Shuo; Feng, Jing; Wei, Si; Qian, Xuehan; Cao, Jie; Chen, Bao-yuan

doi:10.1007/s11325-015-1190-2

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…As showed in the current study, rats with CIH had significantly higher LV‐end‐systolic volume, decreased both fractional shortening and ejection fraction, which are generally associated with ventricular remodeling. Consistent with our results, cardiac dysfunction and LV remodeling were reported to show a significant decrease in LV fractional shortening and ejection fraction in rats treated with intermittent hypoxia (IH) for 4 weeks . In another study, OSA patients with hypertension had decreased LVEF, and FS compared with the nonhypertensive OSA group, suggesting that hypertension acts as a catalyst on CIH‐induced LV systolic dysfunction.…”

Section: Discussionsupporting

confidence: 88%

Hydrogen gas reduces chronic intermittent hypoxia‐induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation

Guan

Lin

Yang

et al. 2018

J of Cellular Biochemistry

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Molecular hydrogen is reported to be used medically to ameliorate various systemic pathological conditions. This study aimed to investigate the effect of hydrogen (H 2 ) gas on hypertension induced by intermittent hypoxia in rats. The adult rats were exposed to chronic intermittent hypoxia (CIH) 8 hours/day for 5 weeks and/or H 2 gas 2 hours/day. We found that the systolic and diastolic blood pressure (BP) increased significantly in rats exposed to intermittent hypoxia, both of which were markedly attenuated after H treatment. Furthermore, intermittent hypoxia exposure elevated renal sympathetic nerve activity, consistent with plasma norepinephrine. Additionally, H 2 gas significantly improved CIH-induced abnormal vascular relaxation. Nevertheless, inhalation of H 2 gas alone did not cause such changes. Moreover, H 2 gas-treated rats exposed to CIH showed a significant reduction in 8-hydroxy-2 deoxyguanosine content and increases in superoxide dismutase activity, indicating improved oxidative stress. Taken together, these results indicate that H 2 gas has significant effects on the reduction of BP without any side effects. Mechanistically, inhibition of sympathetic activity and reduction of systemic vascular resistance may participate in this process via the antioxidant activity of H 2 . K E Y W O R D S chronic intermittent hypoxia, hydrogen, hypertension, sympathetic nerve activity, vasodilator responses J Cell Biochem. 2019;120:3998-4008. wileyonlinelibrary.com/journal/jcb 3998 |

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Section: Discussionsupporting

confidence: 88%

Hydrogen gas reduces chronic intermittent hypoxia‐induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation

Guan

Lin

Yang

et al. 2018

J of Cellular Biochemistry

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“…In addition, the nitric oxide synthase gene deletion via gene knockout showed that the number of apoptotic myocardial cells was decreased and LVEF was increased after myocardial infarction, suggesting that the improvement of cardiac function in heart failure is closely related to the decrease of frequency of myocardial cell apoptosis away from the infarcted zone, and the myocardial cell apoptosis away from the infarcted zone may be one of the important reasons for cardiac remodeling and development of heart failure after myocardial infarction (20). In heart failure, the hypoxia-ischemia of myocardial cells, oxidative stress, inflammatory factors, mechanical load and neuroendocrine factors, can induce myocardial cell apoptosis (21,22), but which factor dominates in heart failure remains unclear, and the specific mechanism of myocardial apoptosis and relationship need to be further studied. At present, animal experiments and autopsy of patients with heart failure have shown that myocardial cell apoptosis exists in heart failure, but the proportion of apoptosis varies in different studies.…”

Section: Discussionmentioning

confidence: 99%

Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats

et al. 2018

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The effects of berberine on cardiac function of heart failure after myocardial infarction and its possible mechanism were investigated. The anterior descending branches of 50 female Wistar rats were ligatured to establish the model of heart failure after myocardial infarction. At 4 weeks after successful modeling, the rats were randomly divided into two groups receiving 4-week gavage with saline (Sal group) and berberine (Ber group), while the sham-operation group (Sham group) was set up. After 4 weeks, the hemodynamics and serum BNP in rats were measured. The hearts of rats were taken to detect the degree of myocardial fibrosis. The myocardial cell apoptosis was detected. The expressions and changes in myocardial apoptosis-related proteins, including Bcl-2, Bax and caspase-3, were detected. The expression and changes in GRP78, CHOP and caspase-12 in myocardial tissue were detected. The results showed that Berberine improved the cardiac function of rats after myocardial infarction. After myocardial infarction, myocardial fibrosis and apoptosis were observed around the infarction area, berberine improved the myocardial fibrosis and reduced cell apoptosis. Furthermore, berberine alleviated endoplasmic reticulum stress (ERS) after myocardial infarction. In conclusion, Berberine can inhibit the myocardium cell apoptosis of heart failure after myocardial infarction, and its mechanism may be realized by affecting the ERS in myocardial tissue of heart failure after myocardial infarction and CHOP and caspase-12 apoptotic signaling pathway, upregulating Bcl-2/Bax expression and downregulating caspase-3 expression, thus inhibiting the cardiac remodeling and protecting the cardiac function.

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“…Hypoxia can lead to oxidative stress and overproduction of reactive oxygen species. Reactive oxygen species can also activate nuclear transcriptional factors, including NF-kB and HIF-1α [17] , which stimulates production of inflammatory mediators such as interleukin (IL)-6 [18] , as we observed in this model.…”

Section: Discussionmentioning

confidence: 89%

Chronic intermittent hypoxia induces cardiac inflammation and dysfunction in a rat obstructive sleep apnea model

Qin

Bian

et al. 2016

J Biomed Res

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Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea (OSA). We used a well-described OSA rat model induced with simultaneous intermittent hypoxia. Male Sprague Dawley rats were individually placed into plexiglass chambers with air pressure and components were electronically controlled. The rats were exposed to intermittent hypoxia 8 hours daily for 5 weeks. The changes of cardiac structure and function were examined by ultrasound. The cardiac pathology, apoptosis, and fibrosis were analyzed by H&E staining, TUNNEL assay, and picosirius staining, respectively. The expression of inflammation and fibrosis marker genes was analyzed by quantitative real-time PCR and Western blot. Chronic intermittent hypoxia/low pressure resulted in significant increase of left ventricular internal diameters (LVIDs), end-systolic volume (ESV), end-diastolic volume (EDV), and blood lactate level and marked reduction in ejection fraction and fractional shortening. Chronic intermittent hypoxia increased TUNNEL-positive myocytes, disrupted normal arrangement of cardiac fibers, and increased Sirius stained collagen fibers. The expression levels of hypoxia induced factor (HIF)-1α, NF-kB, IL-6, and matrix metallopeptidase 2 (MMP-2) were significantly increased in the heart of rats exposed to chronic intermittent hypoxia. In conclusion, the left ventricular function was adversely affected by chronic intermittent hypoxia, which is associated with increased expression of HIF-1α and NF-kB signaling molecules and development of cardiac inflammation, apoptosis and fibrosis.

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Delayed neutrophil apoptosis mediates intermittent hypoxia-induced progressive heart failure in pressure-overloaded rats

Cited by 14 publications

References 34 publications

Hydrogen gas reduces chronic intermittent hypoxia‐induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation

Hydrogen gas reduces chronic intermittent hypoxia‐induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation

Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats

Chronic intermittent hypoxia induces cardiac inflammation and dysfunction in a rat obstructive sleep apnea model

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