CN115227823A - Cpt1抑制剂在制备预防或治疗高原病的药物中的应用 - Google Patents
Cpt1抑制剂在制备预防或治疗高原病的药物中的应用 Download PDFInfo
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Abstract
本发明公开了CPT1抑制剂在制备预防或治疗高原病的药物中的应用，属于医药领域。通过构建高原低氧小鼠模型对小鼠生存率、肺含水量、脑含水量及心功能等指标进行检测，发现CPT1抑制剂可显著提高小鼠生存率，减轻肺、脑水肿，改善心功能，同时通过抑制CPT1调控心肌代谢模式转换保护机体免受高原低氧损伤，本发明将已知产品CPT1抑制剂Etomoxir、Perhexiline或Oxfenicine用于制备预防或治疗高原病的药物是对既往传统治疗的重要补充，为CPT1抑制剂应用于临床高原病治疗和预防提供理论依据。
Description
技术领域
本发明属于医药领域，特别涉及CPT1抑制剂在制备预防或治疗高原病的药物中的应用。
背景技术
高原病是由低海拔进入高海拔地区时，机体对低氧环境的适应能力不全或失调而导致的综合症。据统计，在我国入海拔4200米以上的高原，普通人群的高原反应发生率为38％–76％，主要表现为头痛、头晕、心慌、气促、乏力、失眠、嗜睡等，重者可发生急性重症高原病，例如高原肺水肿、高原脑水肿及心功能障碍，轻者丧失劳动能力，重者危及生命安全。因此，重视、预防和治疗高原病非常重要。然而，目前针对高原病的治疗方案非常有限，主要为药物治疗、物理治疗及对症治疗等，其中乙酰唑胺被认为是预防高原病最好的药物，但仍收效甚微，部分援藏人员仍出现明显的高原反应，甚至死亡。
高原极端低氧可导致机体代谢模式障碍，肉毒碱棕榈酰转移酶1(Carnitinepalmitoyl transferase1,CPT1)为调控脂肪酸代谢的主要因子，可将脂肪酸转移到线粒体上，而阻断脂肪酸转运可以诱导代谢从脂肪酸氧化磷酸化转换为糖酵解，CPT1抑制剂可否保护机体免受极端缺氧的高原病损伤未见报道。
发明内容
本发明的目的在于提供CPT1抑制剂在制备预防或治疗高原病的药物中的应用，所述CPT1抑制剂选自Etomoxir、Perhexiline和Oxfenicine中的一种或多种。
作为优选，所述药物以Etomoxir、Perhexiline和Oxfenicine中的一种或多种为活性成分，还包含药学上可用的载体。
作为优选，所述CPT1抑制剂通过抑制受试者体内CPT1来抑制脂肪酸氧化。
作为优选，所述药物的剂型包括针剂、注射剂、丸剂、颗粒剂、片剂、胶囊剂。
作为优选，所述药物以Etomoxir为活性成分，剂量为0.1–1mg/kg/3天，采用肌肉注射的方式，周期为14–28天。
作为优选，所述药物以Perhexiline为活性成分，剂量为100–300mg/kg/3天，采用口服的方式，周期为14–28天。
作为优选，所述药物以Oxfenicine为活性成分，剂量为100–200mg/kg/3天，采用口服的方式，周期为14–28天。
高原低氧引起代谢模式转换是机体适应环境转变的重要调控方式，可由脂肪酸为主的代谢模式转换为糖酵解为主，CPT1转运脂肪酸进入线粒体参与氧化磷酸化，而阻断CPT1则可抑制线粒体氧化磷酸化，促进糖酵解。本发明将已知产品CPT1抑制剂在制备预防或治疗高原病的药物，通过抑制CPT1调控心肌代谢模式转换，减轻高原低氧损伤，保护心脏功能，提高小鼠生存率，减轻高原肺水肿、高原脑水肿。通过构建高原低氧小鼠模型对小鼠生存率、肺含水量、脑含水量及心功能等指标进行检测，发现CPT1抑制剂可显著提高小鼠生存率，减轻肺、脑水肿，改善心功能，对高原低氧损伤具有保护作用，是对既往传统治疗的重要补充，可以通过调控代谢模式转换保护机体免受高原低氧损伤，为CPT1抑制剂应用于临床高原病治疗和预防提供理论依据。
附图说明
图1是实施例1中平原条件和高原低氧条件下各组小鼠生存曲线。
图2是实施例2中高原6000米干预2周后肺含水量(A)和高原6000米干预2周后脑含水量(B)检测结果。
图3是实施例3中心超代表图(A)、心率(BPM)(B)、左室射血分数(％)(C)和左室缩短分数(％)(D)检测结果。
具体实施方式
为使本发明实施例的目的、技术方案和优点更加清楚，下面将结合本发明实施例的附图对本发明实施例的技术方案进行清楚、完整地描述。显然，所描述的实施例是本发明的一部分实施例，而不是全部的实施例。基于所描述的本发明的实施例，本领域普通技术人员在无需创造性劳动的前提下所获得的所有其它实施例，都属于本发明保护的范围。
Etomoxir，分子结构为
分子式为C17H23ClO4，CAS号为124083–20–1，是可渗透入细胞的不可逆的肉碱棕榈酰基转移酶(CPT)-1和二酰基甘油酰基转移酶(DGAT)抑制剂，也是线粒体CPT1的强抑制剂和抗糖尿病药物的候选药物。
Perhexiline，分子结构为
分子式为C19H35N，CAS号为6621–47–2。
Oxfenicine，分子结构为
分子式为C8H9NO3，CAS号为32462–30–9。
以下实施例中采用的CPT1抑制剂Etomoxir、Perhexiline和Oxfenicine以及其他未注明的材料或试剂均市售可得。
实施例1
本实施例选用SPF级雄性C57/B6小鼠(购自上海杰思捷实验动物有限公司)，周龄为6–8周，体重20g，构建高原低氧损伤模型(6000米高原环境干预2周)，并将小鼠分为八组，设置CPT-1抑制剂处理组和生理盐水对照组，对照组每隔3天腹腔注射生理盐水200uL，处理组每隔3天使用200uL CPT1抑制剂Etomoxir药物(0.5mg/kg/3天，腹腔注射)、Perhexiline(200mg/kg/3天，灌胃)及Oxfenicine(150mg/kg/3天，灌胃)，注射时间为术前14天持续至术后14天，通过记录小鼠生存情况、肺、脑水肿程度，心脏超声等评估小鼠的生存率、肺、脑和心脏功能。实验方案得到复旦大学动物管理与伦理委员会批准。
实施例2
本实施例用实施例1构建的高原低氧小鼠模型实时监测小鼠在6000米高原环境干预2周下的生存情况，检测各组小鼠在CPT-1抑制剂治疗下的疗效。结果如图1所示，在模拟高原环境下，野生型小鼠生存率显著下降，而CPT-1抑制剂(Etomoxir、Perhexiline和Oxfenicine)可显著改善野生型小鼠的生存率，说明CPT-1抑制剂可保护小鼠免受高原低氧损伤。
实施例3
本实施例用实施例1构建的高原低氧小鼠模型检测高原低氧干预后各组小鼠肺、脑含水量，评估各组小鼠肺、脑水肿程度。结果如图2所示，表明CPT1抑制剂可显著减少小鼠肺、脑含水量，降低肺、脑水肿程度，改善小鼠肺、脑功能。
实施例4
本实施例用实施例1构建的高原低氧小鼠模型通过超声心动图评估各组小鼠心脏功能。异氟烷气麻动物后，当小鼠的心率保持在450–500次/分钟时记录M-mode图像；釆集胸骨旁长轴切面、心尖四腔切面B-Mode图像；取胸骨旁左室短轴，2D超声示左室短轴切面，在乳头肌水平应用M型超声记录左心室运动情况，功能学指标包括：心率(Heart Rate)、左室射血分数(Ejection Fraction，％)及左室缩短分数(Fractional Shortening，％)，比较各组小鼠心脏形态及功能变化。结果如图3所示，表明CPT1抑制剂处理组小鼠心功能指标明显改善。
综上可知，CPT1抑制剂处理组相较于生理盐水对照组小鼠生存率显著提高，高原肺水肿、高原脑水肿显著减轻，心功能明显改善，为CPT-1抑制剂用于制备预防或治疗高原病的药物并应用于临床治疗和预防高原病提供理论依据。
以上所述，仅为本发明的具体实施方式，但本发明的保护范围并不局限于此，任何熟悉本技术领域的技术人员在本发明揭露的技术范围内，可轻易想到变化或替换，都应涵盖在本发明的保护范围之内。因此，本发明的保护范围应所述以权利要求的保护范围为准。
Claims (7)
1.CPT1抑制剂在制备预防或治疗高原病的药物中的应用，所述CPT1抑制剂选自Etomoxir、Perhexiline和Oxfenicine中的一种或多种，其中：
Etomoxir的分子结构为
Perhexiline的分子结构为
Oxfenicine的分子结构为
2.根据权利要求1所述的应用，其特征在于，所述药物以Etomoxir、Perhexiline和Oxfenicine中的一种或多种为活性成分，或者还包含药学上可用的载体。
3.根据权利要求1所述的应用，其特征在于，所述CPT1抑制剂通过抑制受试者体内CPT1来抑制脂肪酸氧化。
4.根据权利要求1所述的应用，其特征在于，所述药物的剂型包括针剂、注射剂、丸剂、颗粒剂、片剂、胶囊剂。
5.根据权利要求1所述的应用，其特征在于，所述药物以Etomoxir为活性成分，剂量为0.1–1mg/kg/3天，采用肌肉注射的方式，周期为14–28天。
6.根据权利要求1所述的应用，其特征在于，所述药物以Perhexiline为活性成分，剂量为100–300mg/kg/3天，采用口服的方式，周期为14–28天。
7.根据权利要求1所述的应用，其特征在于，所述药物以Oxfenicine为活性成分，剂量为100–200mg/kg/3天，采用口服的方式，周期为14–28天。
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Non-Patent Citations (2)
| Title |
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| 白振忠: "高原低氧重塑能量代谢的研究进展", 中国高原医学与生物学杂志, vol. 41, no. 1, pages 13 * |
| 陈芝娟等: "基于网络药理学的护肝清脂片治疗非酒精性脂肪肝病分子机制研究", 中药材, vol. 43, no. 6, pages 1467 * |
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