Inhaled volatile β-caryophyllene is incorporated into the aortic wall and attenuates nicotine-induced aorta degeneration via a CB2 receptor-dependent pathway.
Inhaled volatile β-caryophyllene is incorporated into the aortic wall and attenuates nicotine-induced aorta degeneration via a CB2 receptor-dependent pathway.
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吸入的挥发性 β-石竹烯被纳入主动脉壁，并通过 CB2 受体依赖性途径减轻尼古丁诱导的主动脉变性。
DOI：
10.1016/j.biopha.2022.113423
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
N
中科院分区：
文献类型：
--
作者：
Kishi;C.;Higashihara;M.;Takemoto;Y.;Kamei;M.;Yoshioka;Y.;Matsumura;S.;Yamada;K.;Kobayashi;T.;Matahira;Y.;Moriyama;T.;Zaima;N
β-石竹烯是一种挥发性的双环倍半萜类化合物，从黑胡椒、牛至、罗勒、迷迭香、肉桂和丁香等香料中提取的精油中发现。BCP是大麻素受体2(CB2受体)的选择性激动剂，口服BCP具有抗炎、抗氧化和神经保护等多种生物活性。然而，挥发性的BCP如何影响活的生物体仍不清楚。我们之前曾报道吸入BCP会转移到小鼠的血清和器官中；此外，代谢组学分析显示，吸入BCP会影响小鼠肝脏中代谢物的动力学。这些数据表明，吸入BCP可能通过刺激生物系统而影响几种生物活动。在这项研究中，我们评估了BCP吸入对尼古丁诱导的主动脉壁退变的影响。在吸入挥发性BCP的那组小鼠中，尼古丁诱导的弹性纤维降解和基质金属蛋白酶-2(MMP2)阳性区域的增加被减弱。此外，BCP改善了尼古丁诱导的主动脉僵硬和主动脉破裂的易感性。在培养的主动脉上，CB2受体阻滞剂AM630可抑制BCP的抑制作用。这些结果表明，吸入的BCP被结合到主动脉壁中，并通过CB2受体依赖的途径防止尼古丁诱导的主动脉退行性变。
β-caryophyllene (BCP) is a volatile bicyclic sesquiterpenoid found in essential oils obtained from several spices such as black pepper, oregano, basil, rosemary, cinnamon, and clove. BCP is a selective agonist of cannabinoid receptor 2 (CB2 receptor), and orally administered BCP exhibits various biological activities, including anti-inflammatory, antioxidant, and neuroprotective effects. However, it is still unclear how volatile BCP affects living organisms. We previously reported that inhaled BCP is transferred to sera and organs in mice; additionally, metabolomic analysis revealed inhaled BCP affect the dynamics of metabolites in the livers of mice. These data suggest that inhaled BCP may affect several biological activities by stimulating biological systems. In this study, we evaluated the effects of BCP inhalation on nicotine-induced degeneration of the aortic wall. In the group of mice which inhaled volatile BCP, nicotine-induced increases in elastic fiber degradation and matrix metalloproteinase-2 (MMP-2)-positive areas were attenuated. In addition, BCP improved the nicotine-induced stiffness of aortae and vulnerability to aortic rupture. In cultured aortae, the suppressive effects of BCP were inhibited by the CB2 receptor inhibitor AM630. These results suggest that inhaled BCP is incorporated into the aortic wall and prevents nicotine-induced degeneration of the aorta via a CB2 receptor-dependent pathway.
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