Purified ACE attenuates smokeless tobacco-induced increase in macromolecular efflux from the oral mucosa.
Purified ACE attenuates smokeless tobacco-induced increase in macromolecular efflux from the oral mucosa.
复制标题
纯化的 ACE 可减弱无烟烟草引起的口腔粘膜大分子流出的增加。
DOI：
10.1152/jappl.1997.83.1.74
复制
发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Rubinstein,I
中科院分区：
文献类型：
--
作者：
Gao,XP;Suzuki,H;Olopade,CO;Pakhlevaniants,S;Rubinstein,I
放大图片作者：Hedeyuki Suzuki，Christopher O. Olopade，Sergei Pakhlevaniants，and Israel Rubinstein.Purified ACE attenuates smokeless tobacco-induced increase in molecular efflux from the oral mucosal.J. Appl. Physiol.83（1）：74-81，1997.-本研究的目的是确定纯化的血管紧张素I转换酶（ACE）是否减弱无烟烟草提取物（STE）诱导的大分子流出增加原位口腔粘膜。通过活体显微镜观察，我们发现无烟烟草水提取物的窒息引起显著的浓度依赖性渗漏部位形成和荧光素异硫氰酸酯标记的葡聚糖（摩尔质量，70 kDa）从仓鼠颊囊的清除增加（P< 0.05）。纯化兔肺ACE灌胃可明显减弱上述反应，并呈浓度依赖性（P< 0.05）。这些影响是具体的，因为纯化的ACE也显着衰减缓激肽，这是在眼袋中产生的窒息的STE引起的大分子外排的增加，但没有衰减引起的腺苷增加。此外，热灭活的纯化ACE和纯化的超氧化物歧化酶的sufficiency对STE和缓激肽诱导的反应没有显着影响。总的来说，这些数据表明，外源性ACE减弱ST诱导的增加大分子流出的原位口腔粘膜，在一定程度上，通过促进局部缓激肽catalysts。
Gao, Xiao-pei, Hideyuki Suzuki, Christopher O. Olopade, Sergei Pakhlevaniants, and Israel Rubinstein.Purified ACE attenuates smokeless tobacco-induced increase in macromolecular efflux from the oral mucosa.J. Appl. Physiol.83(1): 74–81, 1997.—The purpose of this study was to determine whether purified angiotensin I-converting enzyme (ACE) attenuates smokeless tobacco extract (STE)-induced increase in macromolecular efflux from the in situ oral mucosa. By using intravital microscopy, we found that suffusion of an aqueous extract of smokeless tobacco elicited significant concentration-dependent leaky site formation and increase in clearance of fluorescein isothiocyanate-labeled dextran (mol mass, 70 kDa) from the hamster cheek pouch (P< 0.05). Suffusion of purified rabbit lung ACE significantly attenuated these responses in a concentration-dependent fashion (P< 0.05). These effects were specific because purified ACE also significantly attenuated the increase in macromolecular efflux elicited by bradykinin, which is produced in the cheek pouch during suffusion of STE, but did not attenuate the increase elicted by adenosine. Moreover, suffusion of heat-inactivated purified ACE and purified superoxide dismutase had no significant effects on STE- and bradykinin-induced responses. Collectively, these data suggest that exogenous ACE attenuates STE-induced increase in macromolecular efflux from the in situ oral mucosa, in part, by promoting local bradykinin catabolism.