• The Korean Journal of Physiology and Pharmacology
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• v.13 no.5
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• pp.385-392
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• 2009

Angiotensin II (Ang II) plays an important role in vascular hypertension. The role of the chemokine CCL5 on Ang II-induced activities in vascular smooth muscle cells (VSMCs) has not been studied. In this study, we elucidated the effect of CCL5 on Ang II-induced 12-lipoxygenase (LO) expression and cell proliferation in spontaneously hypertensive rats (SHR) VSMCs. CCL5 decreased Ang II-induced 12-LO mRNA expression and protein production, and it increased Ang II type 2 ($AT_2$) receptor expression in SHR VSMCs. The inhibitory effect of CCL5 on Ang II-induced 12-LO mRNA expression was mediated through the $AT_2$ receptor. Although treatment of CCL5 alone induced SHR VSMCs proliferation, CCL5 inhibited Ang II-induced VSMCs proliferation and PD123,319, an $AT_2$ receptor antagonist, blocked the inhibitory effect of CCL5 on Ang II-induced VSMCs proliferation. Phosphorylation of p38 was detected in VSMCs treated with Ang II or CCL5 alone. But, decrease of p38 phosphorylation was detected in VSMCs treated with Ang II and CCL5 simultaneously (Ang II/CCL5) and PD123,319 increased p38 phosphorylation in VSMCs treated with Ang II/CCL5. Therefore, these results suggest that the inhibitory effect of CCL5 on Ang II-induced VSMCs proliferation is mediated by the $AT_2$ receptor via p38 inactivation, and CCL5 may play a beneficial role in Ang II-induced vascular hypertension.

• Journal of Sensor Science and Technology
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• v.22 no.1
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• pp.76-83
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• 2013

A real-time wireless monitoring and analysis methods using the wearable PPG sensor to estimate cardiovascular condition is studied for ubiquitous healthcare service. A small size and low-power consuming wearable photoplethysmogram (PPG) sensor is designed as a wrist type device and connected with the IP node assigned its own IPv6 address. The measured PPG waveform in the IP node is collected and transferred to a central server PC through the IP-enabled wireless network for storage and analysis purposes. A monitoring and analysis program is designed to process the accelerated plethysmogram (APG) waveform by applying the second order derivatives to analyze systolic waves as well as heart rate variability analysis from the measured PPG waveform. From our results, the features of cardiovascular condition from individual's PPG waveform and estimation of vascular compliance by the comparison of APG-aging index (AI) and ratio of LF/HF are demonstrated.

• Food Science of Animal Resources
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• v.37 no.6
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• pp.917-925
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• 2017

Whey protein, a by-product of milk curdling, exhibits diverse biological activities and is used as a dietary supplement. However, its effects on stress-induced vascular aging have not yet been elucidated. In this study, we found that whey protein significantly inhibited the Ang II-primed premature senescence of vascular smooth muscle cells (VSMCs). In addition, we observed a marked dose- and time-dependent increase in SIRT1 promoter activity and mRNA in VSMCs exposed to whey protein, accompanied by elevated SIRT1 protein expression. Ang II-mediated repression of SIRT1 level was dose-dependently reversed in VSMCs treated with whey protein, suggesting that SIRT1 is involved in preventing senescence in response to this treatment. Furthermore, resveratrol, a well-defined activator of SIRT1, potentiated the effects of whey protein on Ang II-primed premature senescence, whereas sirtinol, an inhibitor of SIRT1, exerted the opposite. Taken together, these results indicated that whey protein-mediated upregulation of SIRT1 exerts an anti-senescence effect, and can thus ameliorate Ang II-induced vascular aging as a dietary supplement.

• Journal of Magnetics
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• v.16 no.3
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• pp.259-262
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• 2011

Compared to acupuncture, the pulsed magnetic field (PMF) stimulus is a useful tool for treatment of many physical conditions and health maintenance due to its advantages as a noninvasive and nontoxic medical treatment. The purpose of this study was to investigate the effect of PMF stimulus direction at PC9 on the alpha activity of electroencephalogram (EEG) and vascular aging calculated from photoplethysmograph (PPG). It can be concluded that the direction of PMF stimulus affects the increase of alpha activity of EEG and PPG, indicating the vascular stiffness and the sclerosis level of blood vessels weakly relevant to the direction of PMF stimulus.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.6
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• pp.1576-1580
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• 2007

Aralia cordata Thunb. (Araliaceae, ACT) is an remarkable herbal plant that has been widely used in traditional oriental medicine for the treatment of inflammatory diseases and cardiovascular disorders. In this study, we have established a vascular aging model in rats by orally administrating excessive vitamin $D_2$ (500,000 IU/kg/day) for 4 days followed by feeding high cholesterol diet for 16 weeks and then rats were randomly divided into control group, high cholesterol diet (HCD) group, HCD+ACT (30 mg/kg) and HCD+ACT (60 mg/kg) group. ACT (30, 60) significantly reduced total cholesterol (TC) content compared with HCD, but no significant differences in the serum lipids. Secondly, we measured the serum levels of Oxidized Low-dencity Lipoprotein (OxLDL) and malondialdehyde (MDA) in order to further investigate the anti-vascular aging mechanism of ACT. The results, ACT (30, 60) treatments decreased OxLDL, MDA　content　and increased Cu/Zn superoxide dismutase activity compared with HCD treatments. The results suggested that ACT inhibited OxLDL production rather than serum lipids lowering and that ACT could be used as potential anti-atherosclerotic agent in aged cells.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.1
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• pp.69-79
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• 2020

Aging is one of the risk factors for the development of cardiovascular diseases. During the progression of cellular senescence, cells enter a state of irreversible growth arrest and display resistance to apoptosis. As a flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated the relationship between quercetin-induced apoptosis and the inhibition of cellular senescence, and determined the mechanism of oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H₂O₂) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated β-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Along with senescence, expression of the anti-apoptotic protein Bcl-2 was observed to increase and the levels of proteins related to the apoptosis pathway were observed to decrease. Quercetin induced apoptosis through the activation of AMP-activated protein kinase. This action led to the alleviation of oxidative stress-induced VSMC senescence. Furthermore, the inhibition of AMPK activation with compound C and siRNA inhibited apoptosis and aggravated VSMC senescence by reversing p53-p21 and p16 pathways. These results suggest that senescent VSMCs are resistant to apoptosis and quercetin-induced apoptosis attenuated the oxidative stress-induced senescence through activation of AMPK. Therefore, induction of apoptosis by polyphenols such as quercetin may be worthy of attention for its anti-aging effects.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.5
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• pp.275-280
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• 2008

A brief ischemic insult induces significant protection against subsequent massive ischemic events. The molecular mechanisms known as preconditioning (PC)-induced ischemic tolerance are not completely understood. We investigated whether kinetic changes of cyclooxygenase (COX)-2 during reperfusion time-periods after PC were related to ischemic tolerance. Rats were given PC by occlusion of middle cerebral artery (MCAO) for 10 min and sacrificed after the indicated time-periods of reperfusion (1, 2, 4, 8, 12, 18 or 24 h). In PC-treated rats, focal ischemia was induced by occlusion of MCA for 24 h and brain infarct volume was then studied to determine whether different reperfusion time influenced the damage. We report that the most significant protection against focal ischemia was obtained in rats with 8 h reperfusion after PC. Administration of indomethacin (10 mg/kg, oral) or rofecoxib (5 mg/kg, oral) 48 h prior to PC counteracted the effect of PC. Immunohistochemical analysis showed that COX-2 and HO-l protein were induced in PC-treated rat brain, which was significantly inhibited by rofecoxib. Taken together, we concluded that the kinetic changes of COX-2 expression during the reperfusion period after PC might be partly responsible for ischemic tolerance.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.4
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• pp.407-413
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• 2017

Vascular reactivity can be influenced by the vascular region, animal age, and pathologies present. Prostaglandins (produced by COX-1 and COX-2) play an important role in the contractile response to phenylephrine in the abdominal aorta of young rats. Although these COXs are found in many tissues, their distribution and role in vascular reactivity are not clear. At a vascular level, they take part in the homeostasis functions involved in many physiological and pathologic processes (e.g., arterial pressure and inflammatory processes). The aim of this study was to analyze changes in the contractile response to phenylephrine of thoracic/abdominal aorta and the coronary artery during aging in rats. Three groups of rats were formed and sacrificed at three distinct ages: prepubescent, young and old adult. The results suggest that there is a higher participation of prostanoids in the contractile effect of phenylephrine in pre-pubescent rats, and a lower participation of the same in old rats. Contrarily, there seems to be a higher participation of prostanoids in the contractile response of the coronary artery of older than pre-pubescent rats. Considering that the changes in the expression of COX-2 were similar for the three age groups and the two tissues tested, and that expression of COX-1 is apparently greater in older rats, COX-1 and COX-2 may lose functionality in relation to their corresponding receptors during aging in rats.

• The Journal of Korean Physical Therapy
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• v.5 no.1
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• pp.79-87
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• 1993

The purpose of this literature review was to identify the physiological changes with aging. The results of this renew were to follows : We have seen a wide variety of such changes in the cells and in all organ systems. 1. At least 40 percent of people over 65 will die of cardiac disease, 15 percent of cerebrovascular disease, and possibly another 5 percent of other types of vascular impairment. 2. The increase rigidity of the thoracic wall and the decreased strength of the expiratory muscles decrease the propulsive effectiveness of the cough. 3. The density of capillaries per motor units is decreased. 4. Starting before age 40 in both sexes there is a shift from an increase in bone mass to a progressive decrease. 5. Histologic studies show a lim age-correlated decrease in the number of Pacini's. Merkel's, and Meissner's corpuscles.

• Food Science of Animal Resources
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• v.40 no.1
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• pp.106-117
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• 2020

Cellular senescence is associated with age-related vascular disorders and has been implicated in vascular dysfunctions. Here, we show that duck oil-loaded nanoemulsion (DO-NE) attenuates premature senescence of vascular smooth muscle cells (VSMCs) triggered by angiotensin II (Ang II). Compared with control nanoemulsion (NE), DO-NE significantly inhibited the activity of senescence-associated β-galactosidase, which is a biomarker of cellular senescence, in Ang II-treated VSMCs. SIRT1 protein expression was dose- and time-dependently induced in VSMCs exposed to DO-NE, but not in those exposed to NE, and SIRT1 promoter activity was also elevated. Consistently, DO-NE also dose-dependently rescued Ang II-induced repression of SIRT1 expression, indicating that SIRT1 is linked to the anti-senescence action of DO-NE in VSMCs treated with Ang II. Furthermore, the SIRT1 agonist resveratrol potentiated the effects of DO-NE on VSMCs exposed to Ang II, whereas the SIRT1 inhibitor sirtinol elicited the opposite effect. These findings indicate that DO-NE inhibits senescence by upregulating SIRT1 and thereby impedes vascular aging triggered by Ang II.