He D.-H.,Xiamen University |
He D.-H.,Fujian Medical University |
Zhang L.-M.,Fujian Medical University |
Lin L.-M.,Affiliated Hospital of Putian College |
And 4 more authors.
International Journal of Molecular Medicine | Year: 2014
Prehypertension has been associated with adverse cerebrovascular events and brain damage. The aims of this study were to investigate ?) whether short- and long-term treatments with losartan or amlodipine for prehypertension were able to prevent blood pressure (BP)-linked brain damage, and ?) whether there is a difference in the effectiveness of treatment with losartan and amlodipine in protecting BP-linked brain damage. In the present study, prehypertensive treatment with losartan and amlodipine (6 and 16 weeks treatment with each drug) was performed on 4-week-old stroke-prone spontaneously hypertensive rats (SHRSP). The results showed that long-term (16 weeks) treatment with losartan is the most effective in lowering systolic blood pressure in the long term (up to 40 weeks follow-up). Additionally, compared with the amlodipine treatment groups, the short- and long-term losartan treatments protected SHRSP from stroke and improved their brains structurally and functionally more effectively, with the long-term treatment having more benefits. Mechanistically, the short- and long-term treatments with losartan reduced the activity of the local renin-angiotensin-aldosterone system (RAAS) in a time-dependent manner and more effectively than their respective counterpart amlodipine treatment group mainly by decreasing AT1R levels and increasing AT2R levels in the cerebral cortex. By contrast, the amlodipine treatment groups inhibited brain cell apoptosis more effectively as compared with the losartan treatment groups mainly through the suppression of local oxidative stress. Taken together, the results suggest that long-term losartan treatment for prehypertension effectively protects SHRSP from stroke-induced brain damage, and this protection is associated with reduced local RAAS activity than with brain cell apoptosis. Thus, the AT1R receptor blocker losartan is a good candidate drug that may be used in the clinic for long-term treatment on prehypertensive populations in order to prevent BP-linked brain damage.
PubMed | Affiliated Hospital of Putian College, Fujian Medical University, Fujian Institute of Hypertension and Peoples Hospital of Ningdu County
Type: Journal Article | Journal: Acta Cardiologica Sinica | Year: 2016
The purpose of this study was to evaluate the effects of prehypertensive losartan and amlodipine administration on left ventricular (LV) remodeling and function in spontaneously hypertensive rats-stroke prone (SHRSP).Spontaneously hypertensive rats-stroke prone were prehypertensively administered losartan, amlodipine, or vehicle. Wistar-Kyoto rats were used as a control. Blood pressure of the rats was determined by tail-cuff method, and LV structure and function were measured by echocardiography and LV cannulation. Collagen volume fraction was analyzed by picrosirius red staining. Protein expressions of brain natriuretic peptide (BNP) and angiotensin II type 1 (AT1R) and type 2 (AT2R) receptors were determined by use of the Western blotting method.Although both drugs downregulated BNP protein expression, the LV remodeling and function were more improved with losartan than with amlodipine treatment. Losartan upregulated AT1R and downregulated AT2R protein expression.Both drugs inhibited LV remodeling and improved LV function in prehypertensively treated SHRSP. Losartan provided better continued heart protection, potentially due to its persistent inhibition of AT1R and activation of AT2R in the myocardium.Amlodipine; Blood pressure; Heart; Losartan; Prehypertension.
Zeng Y.,North Zhongshan Road |
Zeng Y.,Fujian Medical University |
Hong M.,Traditional Chinese Medicine Hospital of Zhangzhou City |
Zhang H.,Fujian Medical University |
And 6 more authors.
Respirology | Year: 2010
Transbronchoscopic balloon detection and selective bronchial occlusion were applied in the management of 40 patients with intractable pneumothorax. An autologous blood clot was used as a bronchial sealant. The efficacy of the procedure, effect on oxygenation and radiographic changes in occluded areas of the lung were evaluated. Background and objective: The aim of this study was to evaluate the efficacy, complications and safety of the application of transbronchoscopic balloon detection (TBD) and selective bronchial occlusion (SBO) to intractable pneumothorax. Methods: Forty patients with pneumothorax, who had experienced more than 7 days of chest tube drainage without closure of the pleural fistula, underwent TBD and SBO. In 10 patients, oxygenation and pulse rates were recorded. A thoracic CT scan was performed 10 days after SBO. Results: The bronchi leading to the pleural fistula were located by TBD in 34 of 40 patients (85%). The air leakages ceased after the first occlusion in 30 patients, and five of these 30 patients underwent a second occlusion due to recurrence of pneumothorax 72 h after the first occlusion. In three of these patients, air leakages ceased after the second occlusion, while the remaining two patients underwent thoracoscopy. In total, 28 of 40 patients (70%) were cured using SBO. During TBD/SBO, the lowest SaO2 was 89.0 ± 2.8%, the mean SaO2 was 93.4 ± 2. 6% and the percentage of time during the procedure that SaO2 was <90% was 10.7 ± 17.5%. Ten days after SBO, thoracic CT scans were performed on 10 patients and no obstructive atelectasis was detected in any patient. Conclusions: These results indicate that TBD and SBO are safe and effective procedures for treating patients with intractable pneumothorax. © 2009 Asian Pacific Society of Respirology.
Liu L.,Fujian Medical University |
Zhang M.,Fujian Medical University |
Li L.,Affiliated Hospital of Putian College |
Li C.,Affiliated Hospital of Putian College |
And 2 more authors.
Gynecologic and Obstetric Investigation | Year: 2014
Aim: To investigate the expression and clinical significance of ATP-binding cassette transporter 1 (ABCA1) in pregnant women with preeclampsia (PE). Methods: 52 pregnant women with PE who were admitted for delivery were enrolled in the study, while 30 normal pregnant inpatients were chosen as controls. Blood lipid and serum ABCA1 concentrations were assayed by enzymatic analysis and ELISA, respectively, and the expression of the ABCA1 gene and its encoded protein were detected and quantified by RT-PCR and Western blotting. Results: In the study group, blood lipid levels were significantly higher than those in the control group (p < 0.01), while the ABCA1 gene and its encoded protein expression in both serum and placental tissue were lower than that of controls. These differences were highly correlated with disease severity (p < 0.05). In PE patients, serum ABCA1 concentration was positively correlated with ABCA1 protein expression in placental tissue (r = 0.384, p < 0.01) and highdensity lipoprotein level (r = 0.318, p < 0.05), but negatively correlated with low-density lipoprotein level (r = -0.279, p < 0.05). Conclusion: In PE women, expression of ABCA1 was decreased, suggesting that ABCA1 may play an important role in onset of PE by altering blood lipid metabolism. © 2014 S. Karger AG, Basel.
Zhang M.,Capital Medical University |
Zhang M.,Beijing Key Laboratory of Emerging Infectious Diseases |
Zhang J.,Capital Medical University |
Zhang J.,Beijing Key Laboratory of Emerging Infectious Diseases |
And 9 more authors.
Inflammation | Year: 2014
Activation of hepatic stellate cell (HSC) is the central event in liver fibrosis. NS5ATP9 is related to many malignant tumors, but little is known about its function in HSC activation. The aim of this study is to investigate the role of NS5ATP9 in HSC activation in vitro. Genes related to liver fibrosis were detected after NS5ATP9 overexpression or silencing with or without transforming growth factor (TGF)-β1 stimulation in the human HSCs by real-time polymerase chain reaction and western blotting. Cell proliferation, migration, and apoptosis were tested, and the mechanisms underlying the effect of NS5ATP9 on HSC activation were studied. We showed that NS5ATP9 suppressed HSC activation and collagen production, with or without TGF-β1 induction. Also, NS5ATP9 inhibited cell proliferation and migration and promoted apoptosis. Furthermore, NS5ATP9 reduced basal and TGF-β1-mediated Smad3/phosphorylated-Smad3 expression. The existence of a physical complex between NS5ATP9 and Smad3 was illustrated. NS5ATP9 suppresses HSC activation, extracellular matrix production, and promotes apoptosis, in part through reducing Smad3/phosphorylated-Smad3 expression. © 2014, Springer Science+Business Media New York.
Chen X.-H.,Affiliated Hospital of Putian College |
Li R.-Y.,Affiliated Hospital of Putian College |
Zhang G.-D.,Affiliated Hospital of Putian College |
Lin H.-B.,Affiliated Hospital of Putian College |
And 3 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2014
BACKGROUND: Previous studies have found that cholecystokinin octapeptide (CCK-8) can promote the regeneration after sciatic nerve injury in rats, but the exact mechanism remains unclear. OBJECTIVE: To screen effective indicators and analyze the mechanism of CCK-8 promoting sciatic nerve regeneration from the perspective of nerve growth factor and nerve regeneration microenvironment. METHODS: Healthy Sprague-Dawley rats, for the preparation of unilateral sciatic nerve transection injury model, were randomly divided into two groups. In the CCK-8 group, the animal model received intraperitoneal injection of CCK-8 (8 nmol/kg) for consecutive 7 days, while the control group was injected with equal volume of normal saline. The nerve growth factor expression, inducible nitric oxide synthase in the spinal cord, serum superoxide dismutase activity and malondialdehyde concentration, as well as apoptotic cells in spinal cord were all detected. RESULTS AND CONCLUSION: In the CCK-8 group, nerve growth factor expression was higher than that in the control group (P < 0.01), while inducible nitric oxide synthase and the number of apoptotic cells were lower (P < 0.01), serum superoxide dismutase activity was higher but malondialdehyde concentrations was lower (P < 0.01, 0.05). The mechanisms of CCK-8 promoting sciatic nerve regeneration include protecting neurons, anti-apoptosis, inhibiting inflammatory response, anti-NO and anti-oxidation, reducing malondialdehyde, and alleviating free radical damage, as well as stimulating nerve growth factor expression and release.