Mdivi-1 improves cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol by inhibiting excessive mitophagy

XU Yao; YANG Shun; YANG Fei; YANG Ying; YUN Huanjie; TAUSEEF Ahmad; TU Shengfen

doi:10.16016/j.2097-0927.202505075

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Mdivi-1 improves cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol by inhibiting excessive mitophagy

Neuroscience | 更新时间：2025-11-13

- Mdivi-1 improves cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol by inhibiting excessive mitophagy
- Journal of Army Medical University Vol. 47, Issue 21, Pages: 2621-2629(2025)
- 作者机构：
  
  重庆医科大学附属儿童医院麻醉科，国家儿童健康与疾病临床医学研究中心，儿童发育疾病研究教育部重点实验室，儿童神经发育与认知障碍重庆市重点实验室，重庆
- 作者简介：
  
  TU Shengfen， E-mail： 15213324272@163.com
- 基金信息：
  
  the General Project of Clinical Medical Research From National Clinical Research Center for Child Health and Disorders(NCRCCHD-2022-GP-0X);the General Project of Natural Science Foundation of Chongqing(CSTB2023NSCQ-MSX0434)
- DOI：10.16016/j.2097-0927.202505075
  CLC： R619;R741;R977.6
- Received：29 May 2025，
  
  Revised：2025-10-27，
  
  Accepted：28 October 2025，
  
  Published：15 November 2025
- 稿件说明：
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徐瑶，杨顺，杨飞，等.Mdivi-1通过抑制过度线粒体自噬改善低氧复合丙泊酚引起的未成熟SD大鼠认知功能障碍［J］.陆军军医大学学报，2025，47（21）：2621-2629.DOI：10.16016/j.2097-0927.202505075.

XU Y，YANG S，YANG F，et al.Mdivi-1 improves cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol by inhibiting excessive mitophagy［J］.J Army Med Univ，2025，47（21）：2621-2629.DOI：10.16016/j.2097-0927.202505075.
徐瑶，杨顺，杨飞，等.Mdivi-1通过抑制过度线粒体自噬改善低氧复合丙泊酚引起的未成熟SD大鼠认知功能障碍［J］.陆军军医大学学报，2025，47（21）：2621-2629.DOI：10.16016/j.2097-0927.202505075. DOI：

XU Y，YANG S，YANG F，et al.Mdivi-1 improves cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol by inhibiting excessive mitophagy［J］.J Army Med Univ，2025，47（21）：2621-2629.DOI：10.16016/j.2097-0927.202505075. DOI：

摘要

目的

探讨线粒体分裂抑制剂1（mitochondrial division inhibitor 1，Mdivi-1）对低氧复合丙泊酚麻醉引起的未成熟SD大鼠认知功能障碍的保护作用。

方法

将72只7日龄SD大鼠［雌雄数量均等，体质量（16.14±3.08）g］按照随机数字表法分为（

=18）：空白对照组（CON组）、抑制剂空白对照组（MCON组）、丙泊酚低氧组（PH组）、抑制剂丙泊酚低氧组（MPH组）。提前30 min对MCON组和MPH组分别给予Mdivi-1（2.4 mg/kg）预处理，PH组和MPH组分别给予丙泊酚（50 mg/kg），腹腔注射完成后，将其立即转移至氧浓度为18%的恒温箱内，持续监测直至动物恢复翻正反射后转入常氧环境中饲养，上述操作每天1次，连续7 d。转录组测序筛选差异表达基因（differential expressed genes， DEGs），京都基因与基因组百科全书（Kyoto encyclopedia of genes and gen

omes，KEGG）富集分析对其进行功能分析；Morris水迷宫行为学试验检测空间学习和记忆功能；HE染色观察海马CA1区神经元形态学变化；透射电镜观察海马神经元内线粒体形态改变；Western blot检测海马组织中Parkin泛素蛋白连接酶（Parkin Rbr E3 ubiquitin protein ligase， Parkin）、PTEN诱导假定激酶1（PTEN-induced putative kinase 1， PINK1）蛋白表达情况。

结果

转录组测序KEGG分析结果：与CON组相比，PH组线粒体自噬通路显著富集。Morris水迷宫试验结果显示：与CON组和MPH组相比，PH组大鼠逃逸潜伏期延长（

0.05），穿越平台次数减少（

0.05），目标象限停留时间缩短（

0.01）。HE染色结果显示：PH组细胞排列紊乱无序，部分区域出现细胞数量锐减的丢失现象，细胞间隙显著增宽；MPH组细胞排列虽也表现出稀疏状态，但相较于PH组，其程度较轻，细胞间隙仅呈现轻微增宽；CON组与MCON组的细胞形态结构良好，轮廓较为清晰，细胞核大小均匀一致，形状均呈圆形。透射电镜结果显示：PH组海马神经元内线粒体肿胀、变形，线粒体嵴紊乱、溶解、消失；MPH组仅部分线粒体肿胀、嵴减少；CON组和MCON组线粒体形态相对完整，基质均匀。Western blot检测结果显示：与CON组相比，PH组SD大鼠海马组织中Parkin、PINK1表达上调（

0.05）；与PH组相比，MPH组SD大鼠海马组织中Parkin、PINK1表达下调（

0.05）。

结论

Mdivi-1可能通过抑制过度线粒体自噬减轻海马神经元损伤进而改善低氧复合丙泊酚引起的未成熟SD大鼠认知功能障碍。

Abstract

Objective

To investigate the protective effect of mitochondrial division inhibitor 1 (Mdivi-1)

a mitophagy inhibitor

on cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol.

Methods

A total of 72 neonatal SD rats (half male and half female

aged 7 d

weighing 16.14±3.08 g) were randomly divided into 4 groups (

=18): blank control group (CON)

Mdivi-1+blank control group (MCON)

propofol+hypoxia group (PH)

and Mdivi-1+propofol+ hypoxia group (MPH). The MCON group and MPH group were pretreated with 2.4 mg/kg Mdivi-1 in 30 min in advance

and subsequently

50 mg/kg propofol was respectively given to the PH group and the MPH group. Immediately after the intraperitoneal injections were completed

the corresponding rats were transferred into a constant temperature chamber containing 18%O

. Then the rats were continuously monitored until resuming the reversing reflex and then transferred to a normoxic environment. The hypoxic treatment was

carried out once per day for 7 consecutive days. Transcriptome sequencing was used to screen for differential expressed genes (DEGs)

and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis was employed to conduct functional analysis. Morris water maze test was applied to exam spatial learning and memory abilities. HE staining was used to observe the morphological changes of neurons in the hippocampal CA1 region. Morphological changes of mitochondria in hippocampal neurons were observed by transmission electron microscopy (TEM). Western blotting was utilized to detect the expression of Parkin Rbr E3 ubiquitin protein ligase (Parkin) and PTEN-induced putative kinase 1 (PINK1) in the hippocampal tissues.

Results

KEGG analysis results indicated that the mitophagy pathway was more significantly enriched in the PH group when compared with the CON group. Morris water maze test revealed that the PH group exhibited obviously prolonged escape latency (

0.05)

reduced frequency of crossing the platform (

0.05)

and shortened residence time in the target quadrant (

0.01) when compared with the CON group and the MPH group. HE staining demonstrated that the cells in the PH group were in disordered arrangement

with great loss in cell count in some areas

and widened intercellular spaces. Although the cell arrangement in the MPH group also showed a sparse state

but the condition was milder than that in the PH group

with slightly widened intercellular space. In the CON group and the MCON group

the cells exhibited round in shape

good morphological structure

relatively clear contours

and uniform cell nuclei. TEM revealed that in the hippocampal neurons of the PH group

the mitochondria were swollen and deformed

and mitochondrial cristae were disordered

dissolved and disappeared. In the MPH group

only some mitochondria were swollen and the cristae were reduced. However

the mitochondrial morphology of the CON and

MCON groups was relatively complete

and the matrix was uniform. Western blot analysis showed that the expression levels of Parkin and PINK1 in the hippocampus were up-regulated in the PH group than the CON group (

0.05)

and reduced in the MPH group than the PH group (

0.05).

Conclusion

Mdivi-1 may reduce hippocampal neuron damage by inhibiting excessive mitophagy and then improve cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol.

关键词

Keywords

references

WU W F ， CHEN C ， LIN J T ， et al . Impaired synaptic plasticity and decreased glutamatergic neuron excitability induced by SIRT1/BDNF downregulation in the hippocampal CA1 region are involved in postoperative cognitive dysfunction ［J］. Cell Mol Biol Lett ， 2024 ， 29 （ 1 ）： 79 . DOI： 10.1186/s11658-024-00595-5 http://dx.doi.org/10.1186/s11658-024-00595-5 .

CZYŻ-SZYPENBEJL K ， MĘDRZYCKA-DĄBROWSKA W ， KWIECIEŃ-JAGUŚ K ， et al . The occurrence of postoperative cognitive dysfunction （POCD）—systematic review ［J］. Psychiatr Pol ， 2019 ， 53 （ 1 ）： 145 - 160 . DOI： 10.12740/PP/90648 http://dx.doi.org/10.12740/PP/90648 .

LIU P F ， ZHAO S ， QIAO H ， et al . Does propofol definitely improve postoperative cognitive dysfunction—a review of propofol-related cognitive impairment ［J］. Acta Biochim Biophys Sin ， 2022 ， 54 （ 7 ）： 875 - 881 . DOI： 10.3724/abbs.2022067 http://dx.doi.org/10.3724/abbs.2022067 .

SCHNEUER F J ， BENTLEY J P ， DAVIDSON A J ， et al . The impact of general anesthesia on child development and school performance： a population-based study ［J］. Paediatr Anaesth ， 2018 ， 28 （ 6 ）： 528 - 536 . DOI： 10.1111/pan.13390 http://dx.doi.org/10.1111/pan.13390 .

LIU L ， GAO W ， YANG S ， et al . Ferritinophagy-mediated hippocampus ferroptosis is involved in cognitive impairment in immature rats induced by hypoxia combined with propofol ［J］. Neurochem Res ， 2024 ， 49 （ 7 ）： 1703 - 1719 . DOI： 10.1007/s11064-024-04128-6 http://dx.doi.org/10.1007/s11064-024-04128-6 .

PARK Y S ， CHOI S E ， KOH H C . PGAM5 regulates PINK1/Parkin-mediated mitophagy via DRP1 in CCCP-induced mitochondrial dysfunction ［J］. Toxicol Lett ， 2018 ， 284 ： 120 - 128 . DOI： 10.1016/j.toxlet.2017.12.004 http://dx.doi.org/10.1016/j.toxlet.2017.12.004 .

CHURILOVA A ， ZACHEPILO T ， BARANOVA K ， et al . Differences in the autophagy response to hypoxia in the hippocampus and neocortex of rats ［J］. Int J Mol Sci ， 2022 ， 23 （ 14 ）： 8002 . DOI： 10.3390/ijms23148002 http://dx.doi.org/10.3390/ijms23148002 .

SUN J ， YU F ， WANG T ， et al . The role of DRP1-PINK1-Parkin-mediated mitophagy in early cadmium-induced liver damage ［J］. Toxicology ， 2022 ， 466 ： 153082 . DOI： 10.1016/j.tox.2021.153082 http://dx.doi.org/10.1016/j.tox.2021.153082 .

YANG S ， XU Y ， AHMAD T ， et al . Mdivi-1 alleviates ferroptosis induced by hypoxia combined with propofol in HT22 cells by inhibiting excessive mitophagy ［J］. Mol Biol Rep ， 2024 ， 51 （ 1 ）： 870 . DOI： 10.1007/s11033-024-09812-y http://dx.doi.org/10.1007/s11033-024-09812-y .

YU S S ， XIN W Q ， JIANG Q L ， et al . Propofol exerts neuroprotective functions by down-regulating microRNA-19a in glutamic acid-induced PC12 cells ［J］. Biofactors ， 2020 ， 46 （ 6 ）： 934 - 942 . DOI： 10.1002/biof.1607 http://dx.doi.org/10.1002/biof.1607 .

LI W X ， LUO R Y ， CHEN C ， et al . Effects of propofol， dexmedetomidine， and midazolam on postoperative cognitive dysfunction in elderly patients： a randomized controlled preliminary trial ［J］. Chin Med J ， 2019 ， 132 （ 4 ）： 437 - 445 . DOI： 10.1097/CM9.0000000000000098 http://dx.doi.org/10.1097/CM9.0000000000000098 .

ZOU L L ， NING M L ， WANG W J ， et al . Naringenin prevents propofol induced neurodegeneration in neonatal mice brain and long-term neurocognitive impacts on adults ［J］. Drug Des Devel Ther ， 2020 ， 14 ： 5469 - 5482 . DOI： 10.2147/DDDT.S280443 http://dx.doi.org/10.2147/DDDT.S280443 .

XING N ， XING F ， LI Y N ， et al . Dexmedetomidine improves propofol-induced neuronal injury in rat hippocampus with the involvement of miR-34a and the PI3K/Akt signaling pathway ［J］. Life Sci ， 2020 ， 247 ： 117359 . DOI： 10.1016/j.lfs.2020.117359 http://dx.doi.org/10.1016/j.lfs.2020.117359 .

于晴，刘阳，孙茫，等 . 低氧因素对丙泊酚麻醉新生大鼠认知功能的影响［J］. 中国临床药理学杂志， 2018 ， 34 （ 14 ）： 1678 - 1681 . DOI： 10.13699/j.cnki.1001-6821.2018.14.027 http://dx.doi.org/10.13699/j.cnki.1001-6821.2018.14.027 .

YU Q ， LIU Y ， SUN M ， et al . Effect of hypoxic factors on cognitive function in propofol-anesthetized neonatal rats ［J］. Chin J Clin Pharmacol ， 2018 ， 34 （ 14 ）： 1678 - 1681 . DOI： 10.13699/j.cnki.1001-6821.2018.14.027 http://dx.doi.org/10.13699/j.cnki.1001-6821.2018.14.027 .

高雯，王维萍，刘玲，等 . 低氧复合丙泊酚通过铁死亡对未成熟SD大鼠海马神经元的影响［J］. 陆军军医大学学报， 2023 ， 45 （ 5 ）： 380 - 385 . DOI： 10.16016/j.2097-0927.202208021 http://dx.doi.org/10.16016/j.2097-0927.202208021 .

GAO W ， WANG W P ， LIU L ， et al . Hypoxia aggravates propofol-induced hippocampal neuron injury in immature SD rats through ferroptosis ［J］. J Army Med Univ ， 2023 ， 45 （ 5 ）： 380 - 385 . DOI： 10.16016/j.2097-0927.202208021 http://dx.doi.org/10.16016/j.2097-0927.202208021 .

张敬，于晴，刘阳，等 . 丙泊酚合并低氧通过p38通路损伤未成熟大鼠的认知功能［J］. 南方医科大学学报， 2018 ， 38 （ 11 ）： 1294 - 1299 . DOI： 10.12122/j.issn.1673-4254.2018.11.03 http://dx.doi.org/10.12122/j.issn.1673-4254.2018.11.03 .

ZHANG J ， YU Q ， LIU Y ， et al . Propofol combined with hypoxia induces cognitive dysfunction in immature rats via p38 pathway ［J］. J South Med Univ ， 2018 ， 38 （ 11 ）： 1294 - 1299 . DOI： 10.12122/j.issn.1673-4254.2018.11.03 http://dx.doi.org/10.12122/j.issn.1673-4254.2018.11.03 .

PALIKARAS K ， LIONAKI E ， TAVERNARAKIS N . Mechanisms of mitophagy in cellular homeostasis， physiology and pathology ［J］. Nat Cell Biol ， 2018 ， 20 （ 9 ）： 1013 - 1022 . DOI： 10.1038/s41556-018-0176-2 http://dx.doi.org/10.1038/s41556-018-0176-2 .

LAZAROU M ， SLITER D A ， KANE L A ， et al . The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy ［J］. Nature ， 2015 ， 524 （ 7565 ）： 309 - 314 . DOI： 10.1038/nature14893 http://dx.doi.org/10.1038/nature14893 .

GEORGAKOPOULOS N D ， WELLS G ， CAMPANELLA M . The pharmacological regulation of cellular mitophagy ［J］. Nat Chem Biol ， 2017 ， 13 （ 2 ）： 136 - 146 . DOI： 10.1038/nchembio.2287 http://dx.doi.org/10.1038/nchembio.2287 .

YAPA N M B ， LISNYAK V ， RELJIC B ， et al . Mitochondrial dynamics in health and disease ［J］. FEBS Lett ， 2021 ， 595 （ 8 ）： 1184 - 1204 . DOI： 10.1002/1873-3468.14077 http://dx.doi.org/10.1002/1873-3468.14077 .

LIANG Y B ， HUANG Y ， SHAO R G ， et al . Propofol produces neurotoxicity by inducing mitochondrial apoptosis ［J］. Exp Ther Med ， 2022 ， 24 （ 4 ）： 630 . DOI： 10.3892/etm.2022.11567 http://dx.doi.org/10.3892/etm.2022.11567 .

GUO P ， MEI J . Exploring the correlation between Drp1 protein and the neurotoxicity of propofol ［J］. Front Neurosci ， 2025 ， 19 ： 1614362 . DOI： 10.3389/fnins.2025.1614362 http://dx.doi.org/10.3389/fnins.2025.1614362 .

CASSIDY-STONE A ， CHIPUK J E ， INGERMAN E ， et al . Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization ［J］. Dev Cell ， 2008 ， 14 （ 2 ）： 193 - 204 . DOI： 10.1016/j.devcel.2007.11.019 http://dx.doi.org/10.1016/j.devcel.2007.11.019 .

SMITH G ， GALLO G . To mdivi-1 or not to mdivi-1： Is that the question ［J］. Dev Neurobiol ， 2017 ， 77 （ 11 ）： 1260 - 1268 . DOI： 10.1002/dneu.22519 http://dx.doi.org/10.1002/dneu.22519 .

OLIVER D ， REDDY P H . Dynamics of dynamin-related protein 1 in Alzheimer’s disease and other neurodegenera-tive diseases ［J］. Cells ， 2019 ， 8 （ 9 ）： 961 . DOI： 10.3390/cells8090961 http://dx.doi.org/10.3390/cells8090961 .

ONG S B ， KWEK X Y ， KATWADI K ， et al . Targeting mitochondrial fission using mdivi-1 in a clinically relevant large animal model of acute myocardial infarction： a pilot study ［J］. Int J Mol Sci ， 2019 ， 20 （ 16 ）： 3972 . DOI： 10.3390/ijms20163972 http://dx.doi.org/10.3390/ijms20163972 .

YANG M J ， LINN B S ， ZHANG Y M ， et al . Mitophagy and mitochondrial integrity in cardiac ischemia-reperfusion injury ［J］. Biochim Biophys Acta Mol Basis Dis ， 2019 ， 1865 （ 9 ）： 2293 - 2302 . DOI： 10.1016/j.bbadis.2019.05.007 http://dx.doi.org/10.1016/j.bbadis.2019.05.007 .

李艳花，张晓娟，张思羽，等 . Mdivi-1通过抑制少突胶质细胞凋亡信号通路发挥髓鞘保护作用［J］. 中国病理生理杂志， 2024 ， 40 （ 3 ）： 527 - 534 . DOI： 10.3969/j.issn.1000-4718.2024.00.011 http://dx.doi.org/10.3969/j.issn.1000-4718.2024.00.011 .

LI Y H ， ZHANG X J ， ZHANG S Y ， et al . Mdivi-1 protects oligodendrocytes through inhibiting apoptotic signaling pathway ［J］. Chin J Pathophysiol ， 2024 ， 40 （ 3 ）： 527 - 534 . DOI： 10.3969/j.issn.1000-4718.2024.00.011 http://dx.doi.org/10.3969/j.issn.1000-4718.2024.00.011 .

铁静静，李晓东，倪子薇，等 . Mdivi-1通过修复黑质网状部线粒体改善肝性脑病小鼠运动功能［J］. 神经解剖学杂志， 2024 ， 40 （ 4 ）： 413 - 420 . DOI： 10.16557/j.cnki.1000-7547.2024.04.002 http://dx.doi.org/10.16557/j.cnki.1000-7547.2024.04.002 .

TIE J J ， LI X D ， NI Z W ， et al . Mdivi-1 improves motor function of mice with hepatic encephalopathy by repairing mitochondrion in substantia nigra Reticulata ［J］. Chin J Neuroanat ， 2024 ， 40 （ 4 ）： 413 - 420 . DOI： 10.16557/j.cnki.1000-7547.2024.04.002 http://dx.doi.org/10.16557/j.cnki.1000-7547.2024.04.002 .

汤春琼，朱娱，王易，等 . 线粒体分裂抑制剂Mdivi-1对脓毒症大鼠肠道屏障功能的保护作用［J］. 陆军军医大学学报， 2024 ， 46 （ 5 ）： 419 - 426 . DOI： 10.16016/j.2097-0927.202303166 http://dx.doi.org/10.16016/j.2097-0927.202303166 .

TANG C Q ， ZHU Y ， WANG Y ， et al . Mitochondrial division inhibitor Mdivi-1 protects intestinal barrier function in septic rats ［J］. J Army Med Univ ， 2024 ， 46 （ 5 ）： 419 - 426 . DOI： 10.16016/j.2097-0927.202303166 http://dx.doi.org/10.16016/j.2097-0927.202303166 .

CHUANG Y C ， LIN T K ， YANG D I ， et al . Peroxisome proliferator-activated receptor-gamma dependent pathway reduces the phosphorylation of dynamin-related protein 1 and ameliorates hippocampal injury induced by global ischemia in rats ［J］. J Biomed Sci ， 2016 ， 23 （ 1 ）： 44 . DOI： 10.1186/s12929-016-0262-3 http://dx.doi.org/10.1186/s12929-016-0262-3 .

胡锦涛，焦晶晶，彭晓红 . Mdivi-1减轻异丙酚诱导的发育期神经元凋亡［J］. 中国医院药学杂志， 2019 ， 39 （ 1 ）： 53 - 56， 71 . DOI： 10.13286/j.cnki.chinhosppharmacyj.2019.01.11 http://dx.doi.org/10.13286/j.cnki.chinhosppharmacyj.2019.01.11 .

HU J T ， JIAO J J ， PENG X H . Mdivi-1 mitigates propofol-induced developmental hippocampal neuroapoptosis in vitro ［J］. Chin J Hosp Pharm ， 2019 ， 39 （ 1 ）： 53 - 56， 71 . DOI： 10.13286/j.cnki.chinhosppharmacyj.2019.01.11 http://dx.doi.org/10.13286/j.cnki.chinhosppharmacyj.2019.01.11 .

LI W L ， JI M L ， LIN Y D ， et al . DEPP/DEPP1/C10ORF10 regulates hepatic glucose and fat metabolism partly via ROS-induced FGF21 ［J］. FASEB J ， 2018 ， 32 （ 10 ）： 5459 - 5469 . DOI： 10.1096/fj.201800357r http://dx.doi.org/10.1096/fj.201800357r .

WU Q ， GAO C ， WANG H C ， et al . Mdivi-1 alleviates blood-brain barrier disruption and cell death in experimental traumatic brain injury by mitigating autophagy dysfunction and mitophagy activation ［J］. Int J Biochem Cell Biol ， 2018 ， 94 ： 44 - 55 . DOI： 10.1016/j.biocel.2017.11.007 http://dx.doi.org/10.1016/j.biocel.2017.11.007 .

MARX N ， RITTER N ， DISSE P ， et al . Detailed analysis of Mdivi-1 effects on complex I and respiratory super complex assembly ［J］. Sci Rep ， 2024 ， 14 （ 1 ）： 19673 . DOI： 10.1038/s41598-024-69748-y http://dx.doi.org/10.1038/s41598-024-69748-y .

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Department of Anesthesiology, National Clinical Research Center of Child Health and Disease, Key Laboratory of Child Developmental Diseases of Ministry of Education, Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University

Department of Anesthesiology, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Child Development and Disorders of Ministry of Education, Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University

State Key Laboratory of Trauma and Chemical Poisoning， Department of Shock and Transfusion， Daping Hospital， Army Medical University

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Department of Nutrition and Food Hygiene, School of Public Health， Guangxi Medical University

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