Bempedoic acid, an ATP-citrate lyase inhibitor, prolongs the golden therapeutic window <italic style="font-style: italic">via</italic> modulating myocardial energy metabolism in rats with uncontrolled hemorrhagic shock

Zhang Qianwei; Zhou Yuanqun; Xiang Xinming; Hu Shiyu; Zeng Anqi; Ouyang Xingnan; Liu Liangming; Li Tao; He Haiyan

doi:10.16016/j.2097-0927.202604100

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Bempedoic acid, an ATP-citrate lyase inhibitor, prolongs the golden therapeutic window via modulating myocardial energy metabolism in rats with uncontrolled hemorrhagic shock

Military Medicine | 更新时间：2026-09-16

- Bempedoic acid, an ATP-citrate lyase inhibitor, prolongs the golden therapeutic window via modulating myocardial energy metabolism in rats with uncontrolled hemorrhagic shock
- Journal of Army Medical University Vol. 48, Issue 17, Pages: 2453-2464(2026)
- 作者机构：
  
  1.陆军军医大学（第三军医大学）大坪医院，护理部，重庆
  2.陆军军医大学（第三军医大学）大坪医院，战伤休克与输血研究室，重庆
  4.陆军军医大学（第三军医大学）大坪医院，麻醉科，重庆
  3.重庆理工大学药学与生物工程学院，重庆
- 作者简介：
  
  Li Tao，E-mail：lt200132@ tmmu.edu.cn
  He Haiyan，E-mail：hehaiyan118@163.com
- 基金信息：
  
  the Key Program of the National Natural Science Foundation of China(82430082)
- DOI：10.16016/j.2097-0927.202604100
  CLC： R322.11;R605.971;R972
- Received：28 April 2026，
  
  Revised：2026-07-13，
  
  Accepted：19 July 2026，
  
  Published：15 September 2026
- 稿件说明：
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张千威，周远群，向鑫明，等.ATP-柠檬酸裂解酶抑制剂贝派地酸通过调控心肌能量代谢延长非控制性失血性休克大鼠黄金救治时间窗［J］.陆军军医大学学报，2026，48（17）：2453-2464.DOI：10.16016/j.2097-0927.202604100.

Zhang Q W，Zhou Y Q，Xiang X M，et al.Bempedoic acid， an ATP-citrate lyase inhibitor， prolongs the golden therapeutic window via modulating myocardial energy metabolism in rats with uncontrolled hemorrhagic shock［J］.J Army Med Univ，2026，48（17）：2453-2464.DOI：10.16016/j.2097-0927.202604100.
张千威，周远群，向鑫明，等.ATP-柠檬酸裂解酶抑制剂贝派地酸通过调控心肌能量代谢延长非控制性失血性休克大鼠黄金救治时间窗［J］.陆军军医大学学报，2026，48（17）：2453-2464.DOI：10.16016/j.2097-0927.202604100. DOI：

Zhang Q W，Zhou Y Q，Xiang X M，et al.Bempedoic acid， an ATP-citrate lyase inhibitor， prolongs the golden therapeutic window via modulating myocardial energy metabolism in rats with uncontrolled hemorrhagic shock［J］.J Army Med Univ，2026，48（17）：2453-2464.DOI：10.16016/j.2097-0927.202604100. DOI：

摘要

目的

ATP-柠檬酸裂解酶（ATP-citrate lyase，ACLY）是介导细胞能量代谢重塑的核心枢纽酶，其特异性抑制剂贝派地酸（bempedoic acid，BA）已在缺血损伤、代谢紊乱相关模型中证实具备多脏器保护作用。本研究旨在明确BA能否延长非控制性失血性休克大鼠的黄金救治时间窗、实现多脏器保护作用，并探究其机制

。

方法

8~10周龄、180~220 g的SPF级SD大鼠，共208只，雌雄各半。采用脾脏纵深切口法建立非控制性失血性休克（uncontrolled hemorrhagic shock，UHS）大鼠模型，大鼠平均动脉压（mean arterial pressure，MAP）降至40 mmHg即为模型建立成功。①48只大鼠采用简单随机抽样法分为3组（

=16），即乳酸林格液（lactated Ringer’s solution，LR）组、10 mg/kg BA组（10 mg/kg BA+LR）、20 mg/kg BA组（20 mg/kg BA+LR）。造模成功后立即进行低压复苏，维持血压50~60 mmHg，观察各组大鼠血压变化、失血率、输液量及低压维持时间。②96只大鼠

按简单随机抽样分为4组（

=24），即假手术（Sham）组、UHS组、LR组、BA组（20 mg/kg BA+LR）。造模成功后，UHS组不实施复苏，其余2组立即行低压复苏，1 h后结扎脾动脉彻底止血并补足2倍失血量的LR进行确定性治疗。检测各组大鼠存活情况、血气指标、肝肾肠血流量、重要器官功能损伤指标、肺脑含水量、心肌收缩功能、心肌组织游离脂肪酸（free fatty acid，FFA）和ATP的含量。

结果

①LR组仅能将MAP稳定维持在50~60 mmHg约60 min，10 mg/kg BA组和20 mg/kg BA组均可稳定维持超过180 min。与LR组相比，20 mg/kg BA组失血率显著降低（63.7%±12.8%

73.8%±4.4%，

0.05），输液量也显著减少［（6.8±4.9）

vs （

18.7±9.8） mL，

0.05］。LR组大鼠的平均低压维持时间为（57±17）min，1 h维持率为68.8%；所有大鼠在80 min内死亡。10 mg/kg BA组和20 mg/kg BA组大鼠的平均低压维持时间分别延长至（138±60）min和（157±50）min，3 h低压维持率分别达50.0%和68.7%。②LR组失血率（55.6%±6.3%）显著高于UHS组（48.4%±5.3%，

0.05）。BA组失血率较LR组显著降低（47.2%±6.0%，

0.05），输液量显著减少［（4.5±2.9）

（15.7±6.4）mL，

0.05］，大鼠72 h存活率由12.5%提升至25.0%（

0.05）。与LR组相比，BA组大鼠血气相关指标包括Hb和PaO

水平显著改善（

0.05）；肝、肾、肠血流量明显恢复（

0.05），接近正常水平；心、肝、肾功能损伤也有所减轻，其中肌钙蛋白I（cardiac troponin I，cTnI）和谷丙转氨酶（alanine aminotransferase，ALT）的水平显著降低（

0.05），但对肺脑含水量的影响无显著性差异。与LR组相比，BA组大鼠血清中的cTnI水平明显降低（

0.05）。LR组大鼠心肌细胞的收缩幅度较UHS组有所恢复，但仅恢复至正常水平的25.8%，BA组大鼠心肌细胞的收缩幅度恢复至正常水平的54.6%（

0.05）。与UHS组相比，LR组大鼠心肌组织中FFA和ATP水平无明显改善作用，BA组大鼠心肌FFA水平显著降低（

0.05），ATP含量提高（

0.05）。

结论

ACLY抑制剂BA能够有效延长非控制性失血性休克大鼠的黄金救治时间窗，其可通过改善机体氧合状态、恢复脏器血流灌注、提升心肌ATP含量以纠正能量代谢紊乱，减轻心肌及肝肾功能损伤，最终提高大鼠72 h存活率。

Abstract

Objective

ATP-citrate lyase (ACLY

)

a pivotal hub enzyme mediating the remodeling of cellular energy metabolism

and its specific inhibitor

bempedoic acid (BA)

has been shown to exert multi-organ protective effects in models of ischemic injury and metabolic disorders. This study aims to determine whether BA could prolong the golden therapeutic window and exert mu

lti-organ protection in a rat model of uncontrolled hemorrhagic shock (UHS)

and to explore its underlying mechanisms.

Methods

A total of 208 SPF-grade SD rats (8 to 10 weeks old

weighing 180 to 220 g

half male and half female) were subjected. A rat UHS model was established by deep cutting the splenic parenchyma

with successful modeling defined as a mean arterial pressure (MAP) decrease to 40 mmHg. ①Forty-eight rats were randomly divided into a lactated Ringer’s solution (LR) group

a 10 mg/kg BA group (10 mg/kg BA + LR)

and a 20 mg/kg BA group (20 mg/kg BA+LR)

with 16 animals in each group. Hypotensive resuscitation was initiated immediately after successful modeling to maintain MAP at 50 to 60 mmHg. Blood pressure profiles

blood loss rate

infusion volume

and duration of maintained hypotension were recorded. ② Ninety-six rats were randomly divided into (

=24): a Sham group

a UHS group

a LR group

and a BA group (20 mg/kg BA+LR). After successful modeling

the UHS group received no resuscitation

while the other 2 groups underwent immediate hypotensive resuscitation. In 1 h later

the splenic artery was ligated for definitive hemostasis

followed by definitive fluid therapy with LR equivalent to twice the total blood loss volume. Outcome measurements included survival status

blood gas parameters

hepatic

renal and intestinal blood perfusion

biomarkers of vital-organ injury

pulmonary and cerebral water contents

myocardial contractile function

as well as myocardial levels of free fatty acid (FFA) and adenosine triphosphate (ATP).

Results

① In the LR group

MAP was stably maintained within 50 to 60 mmHg for approximately 60 min

whereas both 10 and 20 mg/kg BA combined with LR solution sustained the target blood pressure for more than 180 min. Compared with the LR group

the 20 mg/kg BA group exhibited a significantly lower blood loss rate (63.7%±12.8%

73.8%±4.4%

0.05) and reduce

d infusion volume [(6.8±4.9)

(18.7±9.8) mL

0.05

]

. The mean duration of maintained hypotension in the LR group was (57±17) min

with a 1-hour maintenance rate of 68.8%

and all animals died within 80 min. The mean hypotension- maintenance durations were extended to (138±60) min in the 10 mg/kg BA group and (157±50) min in the 20 mg/kg BA group

with 3-hour maintenance rates of 50.0% and 68.7%

respectively. ② The blood loss rate in the LR group was markedly higher than that in the UHS group [(55.6%± 6.3%)

(48.4%±5.3%)

0.05

]

. The BA group demonstrated a significantly lower blood loss rate compared with the LR group (47.2%±6.0%

0.05)

along with a markedly reduced infusion volume [(4.5±2.9)

(15.7±6.4) mL

0.05

]

and the 72-hour survival rate increased from 12.5% to 25.0% (

0.05). Compared with the LR group

BA intervention resulted in significant improvements in blood gas parameters including hemoglobin (Hb) and arterial partial pressure of oxygen (PaO

) (

0.05)

and restored hepatic

renal and intestinal blood perfusion close to normal levels (

0.05). BA treatment also mitigated cardiac

hepatic and renal injuries

with significantly decreased levels of cardiac troponin I (cTnI) and alanine aminotransferase (ALT) (

0.05)

while no significant difference was observed in pulmonary and cerebral water contents. Serum cTnI levels were significantly lower in the BA group than the LR group (

0.05). Cardiomyocyte contraction amplitude in the LR group recovered to only 25.8% of the normal level

whereas BA treatment restored it to 54.6% of normal (

0.05). Compared with the UHS group

the LR group showed no significant improvement in myocardial tissue FFA and ATP levels

whereas the BA group exhibited significantly decreased myocardial FFA le

vels and increased ATP content (both

0.05).

Conclusion

The ACLY inhibitor BA effectively prolongs the golden therapeutic window in UHS rats. Its mechanism may be related to improving systemic oxygenation

restoring visceral perfusion

and enhancing myocardial ATP content to reverse energy metabolic disturbance

thereby alleviating myocardial and hepatic-renal function injuries and ultimately improving the 72-hour survival rate.

关键词

Keywords

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Department of Pathology, West China Hospital of Sichuan University

Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Health, Chongqing Medical Nutrition Research Center, Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University)

State Key Laboratory of Trauma, Burns and Combined Injury, Department of War Wound Shock and Blood Transfusion, Institute of Surgery Research, Daping Hospital, Army Medical University (Third Military Medical University)

State Key Laboratory of Trauma, Burns and Combined Injury, Department of War Wound Shock and Blood Transfusion, Institute of Surgery Research, Army Medical University (Third Military Medical University)

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Bempedoic acid, an ATP-citrate lyase inhibitor, prolongs the golden therapeutic window via modulating myocardial energy metabolism in rats with uncontrolled hemorrhagic shock

DOI：10.16016/j.2097-0927.202604100

摘要

Abstract

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