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논문 기본 정보

자료유형
학술저널
저자정보
Hye Young Kim (Yeungnam University) Hye Ju Cha (Yeungnam University) Jin Hee Choi (Yeungnam University) Young Jin Kang (Yeungnam University) So Young Park (Yeungnam University) Hee Sun Kim (Yeungnam University)
저널정보
대한바이러스학회 JOURNAL OF BACTERIOLOGY AND VIROLOGY Journal of Bacteriology and Virology 제45권 제2호
발행연도
2015.6
수록면
138 - 150 (13page)

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CCL5, a proinflammatory chemokine, has been shown to attenuate angiotensin (Ang) II-induced expression of hypertensive mediators as well as Ang II-induced inhibition of anti-hypertensive mediator expression in vascular smooth muscle cells (VSMCs) of spontaneously hypertensive rats (SHR). In the present study, functional roles of CCL5 on hypertension were examined in developing hypertension state SHR (DHSHR). DHSHR at an age of 8 weeks were injected CCL5 (1.5 μg/kg) subcutaneously twice a day for 3 weeks (SHRi, n=5). Control groups consisted of normal age-matched saline-treated SHR (SHRc, n=5) and normotensive Wistar-Kyoto rats (WKY, n=5). Effect of CCL5 on blood pressure was measured before treatment, weekly during treatment, and 1 day after the final injection. After injecting for 3 weeks, effects of CCL5 on expression of hypertensive mediators were examined in thoracic aorta tissues and VSMCs. Blood pressure in SHRi was maintained without any elevation during the treatment period, whereas blood pressure in SHRc progressively increased with age. Expression of Ang II subtype I receptor was reduced in SHRi thoracic aorta tissues and VSMCs compared to those in SHRc. In addition, expression levels of hypertensive mediators were significantly reduced in SHRi thoracic aorta tissues and VSMCs compared to those in SHRc. In contrast, AMP-activated protein kinase (AMPK) activity and interleukin-10 (IL-10) expression were elevated in SHRi thoracic aorta tissues and VSMCs compared to levels in SHRc. These results suggest that reduction of hypertensive mediators and elevation of antihypertensive mediators by CCL5 treatment promotes maintenance of blood pressure in DHSHR.

목차

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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