杜仲木脂素和醛糖还原酶抑制剂依帕司他对高血压血管重构的影响。

PubMed ID
G H
发表日期 2011年Jan月

原始出处 民族药理学杂志
Journal of ethnopharmacology
作者 Gu  Juan  Wang  Jun-Jie  Yan  Jin  Cui  Chang-Fu  Wu  Wei-Hua  Li  Ling  Wang  Zhen-Shan  Yu  Min  Gao  Na  Liu  Li  Ouyang  Dong-Sheng 

文献标题 杜仲木脂素和醛糖还原酶抑制剂依帕司他对高血压血管重构的影响。
Effects of lignans extracted from Eucommia ulmoides and aldose reductase inhibitor epalrestat on hypertensive vascular remodeling.
Effects of lignans extracted from Eucommia ulmoides and aldose reductase inhibitor epalrestat on hypertensive vascular remodeling.

文献摘要 AIM OF THE STUDY

探讨杜仲木脂素和依帕司他对自发性高血压大鼠血管重构的影响。

MATERIALS AND METHODS

将10周龄雄性自发性高血压大鼠随机分为3组,每组12只,每日灌胃给予卡托普利100mg/kg/d、醛糖还原酶抑制剂依帕司他100mg/kg/d和木脂素300mg/kg/d,共16周。性别、年龄和数量匹配的自发性高血压大鼠和血压正常的Wistar-Kyoto大鼠用蒸馏水(溶媒)作为对照。每周给大鼠称重。采用无创血压监测方法定期测量平均动脉压和心率。实验结束时(26周龄)处死。分离肠系膜上动脉和主动脉,用免疫组织化学方法测定其组织形态和醛糖还原酶的表达。

RESULTS

卡托普利和木脂素可降低自发性高血压大鼠的平均动脉血压,而不是依帕司他。组织形态计量学显示,三个治疗组的血管重构均得到改善。

CONCLUSIONS

木脂素和依帕司他均可逆转高血压血管重构。醛糖还原酶在高血压血管重构的病理过程中起重要作用,而不是在血压升高的病理过程中。提示醛糖还原酶可能成为治疗心血管疾病的新靶点。


AIM OF THE STUDY

To investigate the effects of lignans extracted from Eucommia ulmoides and epalrestat on vascular remodeling in spontaneously hypertensive rats.

MATERIALS AND METHODS

Ten-week-old male spontaneously hypertensive rats were randomly divided into 3 groups (12 rats each group), and treated orally with 100 mg/kg/d of captopril (an angiotensin-converting enzyme inhibitor), 100 mg/kg/d of epalrestat (an aldose reductase inhibitor) and 300 mg/kg/d of lignans by gavage daily for 16 weeks, respectively. Sex-, age-, and number-matched spontaneously hypertensive rats and normotensive Wistar Kyoto rats, were treated with distilled water (vehicle) as controls. The rats were weighed weekly. Mean arterial blood pressure and heart rate were measured periodically by non-invasive blood pressure monitoring. They were sacrificed at the end of experiment (26-week-old). Superior mesenteric artery and aorta were isolated for determination of histomorphometry and the expression of aldose reductase by immunohistochemistry.

RESULTS

Captopril and lignans, but not epalrestat, decreased mean arterial blood pressure in spontaneously hypertensive rats. Vascular remodeling was improved in all three treated groups by histomorphometry.

CONCLUSIONS

Both lignans and epalrestat reversed hypertensive vascular remodeling. Aldose reductase played a vital role in the pathologic process of hypertensive vascular remodeling rather than elevation of blood pressure. These data suggested that aldose reductase could be a new therapeutic target for the treatment of cardiovascular diseases.

AIM OF THE STUDY

To investigate the effects of lignans extracted from Eucommia ulmoides and epalrestat on vascular remodeling in spontaneously hypertensive rats.

MATERIALS AND METHODS

Ten-week-old male spontaneously hypertensive rats were randomly divided into 3 groups (12 rats each group), and treated orally with 100 mg/kg/d of captopril (an angiotensin-converting enzyme inhibitor), 100 mg/kg/d of epalrestat (an aldose reductase inhibitor) and 300 mg/kg/d of lignans by gavage daily for 16 weeks, respectively. Sex-, age-, and number-matched spontaneously hypertensive rats and normotensive Wistar Kyoto rats, were treated with distilled water (vehicle) as controls. The rats were weighed weekly. Mean arterial blood pressure and heart rate were measured periodically by non-invasive blood pressure monitoring. They were sacrificed at the end of experiment (26-week-old). Superior mesenteric artery and aorta were isolated for determination of histomorphometry and the expression of aldose reductase by immunohistochemistry.

RESULTS

Captopril and lignans, but not epalrestat, decreased mean arterial blood pressure in spontaneously hypertensive rats. Vascular remodeling was improved in all three treated groups by histomorphometry.

CONCLUSIONS

Both lignans and epalrestat reversed hypertensive vascular remodeling. Aldose reductase played a vital role in the pathologic process of hypertensive vascular remodeling rather than elevation of blood pressure. These data suggested that aldose reductase could be a new therapeutic target for the treatment of cardiovascular diseases.


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