Welcome to visit Zhongnan Medical Journal Press Series journal website!

Home Articles Vol 37,2024 No.4 Detail

Research progress of the effect of reactive oxygen species on ischemia-reperfusion injury skin flaps and traditional Chinese medicine intervention

Published on Apr. 28, 2024Total Views: 1237 times Total Downloads: 501 times Download Mobile

Author: WEI Xiaotao 1, 2 ZHANG Yuchang 1 HE Zhijun 3 LIU Tao 3 WANG Weiwei 2

Affiliation: 1. Department of Hand Surgery, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou 730000, China 2. Clinical School of Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou 730000, China 3. Department of Foot and Ankle Orthopedics, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou 730000, China

Keywords: Ischaemia-reperfusion injury Reactive oxygen species Skin flaps Traditional Chinese medicine

DOI: 10.12173/j.issn.1004-4337.202312026

Reference: Wei XT, Zhang YC, He ZJ, Liu T, Wang WW. Research progress of the effect of reactive oxygen species on ischemia-reperfusion injury skin flaps and traditional Chinese medicine intervention[J]. Journal of Mathematical Medicine, 2024, 37(4): 287-292. DOI: 10.12173/j.issn.1004-4337.202312026[Article in Chinese]

  • Abstract
  • Full-text
  • References
Abstract

Ischemia-reperfusion injury (IRI) is a disease in which ischemia-like changes occurrs in tissues and organs triggered by inadequate perfusion of tissues and organs, and when the tissues and organs received adequate blood perfusion again, the damage state of the tissues and organs fails to improve, and on the contrary, the damage continues to aggravate, ultimately resulting in necrosis, which is commonly seen in post-transplantation flaps, and multiple organs, such as the liver, kidneys, and brain. The detailed mechanisms of IRI have yet to be fully elucidated, previous studies found that reactive oxygen species (ROS) was an important pathogenetic factor in IRI, and ROS could stimulate the release of pro-inflammatory substances, such as phospholipase A2, tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interferon-γ (IFN-γ), and angiotensin II from IRI tissues, and induce xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase systems, exacerbating local oxidative stress and inflammatory responses, while ROS was involved in apoptosis, autophagy, and necrosis, causing secondary damage to IRI tissues. This paper reviewed the effect of ROS in IRI skin flaps and the progress of traditional Chinese medicine intervention research, in order to provide reference for the development of new therapeutic interventions.

Full-text
Please download the PDF version to read the full text: download
References

1.Pu CM, Chen YC, Chen YC, et al. Interleukin-6 from adipose-derived stem cells promotes tissue repair by the increase of cell proliferation and hair follicles in ischemia/reperfusion-treated skin flaps[J]. Mediators Inflamm, 2019, 2019: 2343867. DOI: 10.1155/2019/2343867.

2.Jahn N, Völker MT, Laudi S, et al. Analysis of volatile anesthetic-induced organ protection in simultaneous pancreas-kidney transplantation[J]. J Clin Med, 2022, 11(12): 3385. DOI: 10.3390/jcm11123385.

3.Chen Z, Wu H, Yang J, et al. Activating parkin-dependent mitophagy alleviates oxidative stress, apoptosis, and promotes random-pattern skin flaps survival[J]. Commun Biol, 2022, 5(1): 616. DOI: 10.1038/s42003-022-03556-w.

4.González-Montero J, Brito R, Gajardo AI, et al. Myocardial reperfusion injury and oxidative stress: therapeutic opportunities[J]. World J Cardiol, 2018, 10(9): 74-86. DOI: 10.4330/wjc.v10.i9.74.

5.Liu H, Wang W, Weng X, et al. The H3K9 histone methyltransferase G9a modulates renal ischemia reperfusion injury by targeting Sirt1[J]. Free Radic Biol Med, 2021, 172: 123-135. DOI: 10.1016/j.freeradbiomed.2021.06.002.

6.Chen G, Shen H, Zang L, et al. Protective effect of luteolin on skin ischemia-reperfusion injury through an AKT-dependent mechanism[J]. Int J Mol Med, 2018, 42(6): 3073-3082. DOI: 10.3892/ijmm.2018.3915.

7.Ornellas FM, Ornellas DS, Martini SV, et al. Bone marrow-derived mononuclear cell therapy accelerates renal ischemia-reperfusion injury recovery by modulating inflammatory, antioxidant and apoptotic related molecules[J]. Cell Physiol Biochem, 2017, 41(5): 1736-1752. DOI: 10.1159/000471866.

8.Ling Q, Yu X, Wang T, et al. Roles of the exogenous H2S-mediated SR-a signaling pathway in renal ischemia/ reperfusion injury in regulating endoplasmic reticulum stress-induced autophagy in a rat model[J]. Cell Physiol Biochem, 2017, 41(6): 2461-2474. DOI: 10.1159/000475915.

9.Torosyan R, Huang S, Bommi PV, et al. Hypoxic preconditioning protects against ischemic kidney injury through the IDO1/kynurenine pathway[J]. Cell Rep, 2021, 36(7): 109547. DOI: 10.1016/j.celrep.2021.109547.

10.Duerr GD, Wu S, Schneider ML, et al. CpG postconditioning after reperfused myocardial infarction is associated with modulated inflammation, less apoptosis, and better left ventricular function[J]. Am J Physiol Heart Circ Physiol, 2020, 319(5): H995-H1007. DOI: 10.1152/ajpheart.00269.2020.

11.Bhargava P, Schnellmann RG. Mitochondrial energetics in the kidney[J]. Nat Rev Nephrol, 2017, 13(10): 629-646. DOI: 10.1038/nrneph.2017.107.

12.Zorov DB, Juhaszova M, Sollott SJ. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release[J]. Physiol Rev, 2014, 94(3): 909-950. DOI: 10.1152/physrev.00026.2013.

13.Wu MY, Yiang GT, Liao WT, et al. Current mechanistic concepts in ischemia and reperfusion injury[J]. Cell Physiol Biochem, 2018, 46(4): 1650-1667. DOI: 10.1159/000489241.

14.Daiber A. Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species[J]. Biochim Biophys Acta, 2010, 1797(6-7): 897-906. DOI: 10.1016/j.bbabio.2010.01.032.

15.Dikalov S. Cross talk between mitochondria and NADPH oxidases[J]. Free Radic Biol Med, 2011, 51(7): 1289-1301. DOI: 10.1016/j.freeradbiomed.2011.06.033.

16.Granger DN, Kvietys PR. Reperfusion injury and reactive oxygen species: the evolution of a concept[J]. Redox Biol, 2015, 6: 524-551. DOI: 10.1016/j.redox.2015.08.020.

17.Battelli MG, Bortolotti M, Bolognesi A, et al. Pro-aging effects of xanthine oxidoreductase products[J]. Antioxidants (Basel), 2020, 9(9): 839. DOI: 10.3390/antiox9090839.

18.Shibuya S, Watanabe K, Ozawa Y, et al. Xanthine oxidoreductase-mediated superoxide production is not involved in the age-related pathologies in Sod1-deficient mice[J]. Int J Mol Sci, 2021, 22(7): 3542. DOI: 10.3390/ijms22073542.

19.Jung HY, Oh SH, Ahn JS, et al. NOX1 inhibition attenuates kidney ischemia-reperfusion injury via inhibition of ROS-mediated ERK signaling[J]. Int J Mol Sci, 2020, 21(18): 6911. DOI: 10.3390/ijms21186911.

20.Cedro RCA, Menaldo DL, Costa TR, et al. Cytotoxic and inflammatory potential of a phospholipase A2 from Bothrops jararaca snake venom[J]. J Venom Anim Toxins Incl Trop Dis, 2018, 24: 33. DOI: 10.1186/s40409-018-0170-y.

21.Kamarauskaite J, Baniene R, Trumbeckas D, et al. Caffeic acid phenethyl ester protects kidney mitochondria against ischemia/reperfusion induced injury in an in vivo rat model[J]. Antioxidants (Basel), 2021, 10(5): 747. DOI: 10.3390/antiox10050747.

22.Xie M, Cho GW, Kong Y, et al. Activation of autophagic flux blunts cardiac ischemia/reperfusion injury[J]. Circ Res, 2021, 129(3): 435-450. DOI: 10.1161/CIRCRESAHA. 120.318601.

23.Li J, Bao G, ALyafeai E, et al. Betulinic acid enhances the viability of random-pattern skin flaps by activating autophagy[J]. Front Pharmacol, 2019, 10: 1017. DOI: 10.3389/fphar.2019.01017.

24.Zhao YG, Zhang H. Autophagosome maturation: an epic journey from the ER to lysosomes[J]. J Cell Biol, 2019, 218(3): 757-770. DOI: 10.1083/jcb.201810099.

25.Liu H, Chen J, Luo W, et al. Vascular anatomy and clinical application of type Ⅲ perforator flap based on the oblique branch of lateral circumflex femoral artery[J]. Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi, 2022, 36(1): 92-97. DOI: 10.7507/1002-1892.202108131.

26.Tirichen H, Yaigoub H, Xu W, et al. Mitochondrial reactive oxygen species and their contribution in chronic kidney disease progression through oxidative stress[J]. Front Physiol, 2021, 12: 627837. DOI: 10.3389/fphys. 2021.627837.

27.Kim YS, Lee HY, Jang JY, et al. Redox treatment ameliorates diabetes mellitus-induced skin flap necrosis via inhibiting apoptosis and promoting neoangiogenesis[J]. Exp Biol Med (Maywood), 2021, 246(6): 718-728. DOI: 10.1177/1535370220974269.

28.Li J, Lou J, Yu G, et al. Targeting TFE3 protects against lysosomal malfunction-induced pyroptosis in random skin flaps via ROS elimination[J]. Front Cell Dev Biol, 2021, 9: 643996. DOI: 10.3389/fcell.2021.643996.

29.Wu C, Lu W, Zhang Y, et al. Inflammasome activation triggers blood clotting and host death through pyroptosis[J]. Immunity, 2019, 50(6): 1401-1411. e4. DOI: 10.1016/j.immuni.2019.04.003.

30.Taverne YJ, Bogers AJ, Duncker DJ, et al. Reactive oxygen species and the cardiovascular system[J]. Oxid Med Cell Longev, 2013, 2013: 862423. DOI: 10.1155/2013/862423.

31.Zhao Y, Zhang Y, Kong H, et al. Carbon dots from paeoniae radix alba carbonisata: hepatoprotective effect[J]. Int J Nanomedicine, 2020, 15: 9049-9059. DOI: 10.2147/IJN.S281976.

32.Balendra V, Singh SK. Therapeutic potential of astaxanthin and superoxide dismutase in Alzheimer's disease[J]. Open Biol, 2021, 11(6): 210013. DOI: 10.1098/rsob.210013.

33.Dudzińska E, Gryzinska M, Ognik K, et al. Oxidative stress and effect of treatment on the oxidation product decomposition processes in IBD[J]. Oxid Med Cell Longev, 2018, 2018: 7918261. DOI: 10.1155/2018/7918261.

34.Jové M, Mota-Martorell N, Pradas I, et al. The advanced lipoxidation end-product malondialdehyde-lysine in aging and longevity[J]. Antioxidants (Basel), 2020, 9(11): 1132. DOI: 10.3390/antiox9111132.

35.魏德华, 刘珑玲, 曾御, 等. 淫羊藿苷缓解腹部皮瓣缺血再灌注损伤模型大鼠的作用及机制研究[J]. 现代生物医学进展, 2022, 22(6): 1024-1027, 1017. [Wei DH, Liu LL, Zeng Y, et al. Effect and mechanism of icariin in alleviating ischemia-reperfusion injury of abdominal flap in rats[J]. Progress in Modern Biomedicine, 2022, 22(6): 1024-1027, 1017.] DOI: 10.13241/j.cnki.pmb.2022.06.005.

36.黄清霞, 覃川娴, 何泽源, 等. 巴戟天化学成分、药理作用及质量标志物预测分析[J]. 中华中医药学刊, 2022, 40(7): 251-258. [Huang QX, Qin CX, He ZY, et al. Chemical components and pharmacological action of bajitian (radix morindae officinalis) and predictive analysis on Q-marker[J]. Chinese Archives of Traditional Chinese Medicine, 2022, 40(7): 251-258.] DOI: 10.13193/j.issn.1673-7717.2022.07.060.

37.Wang C, Mao C, Lou Y, et al. Monotropein promotes angiogenesis and inhibits oxidative stress-induced autophagy in endothelial progenitor cells to accelerate wound healing[J]. J Cell Mol Med, 2018, 22(3): 1583-1600. DOI: 10.1111/jcmm.13434.

38.张燕, 崔欣萍, 王文全, 等. pH对水培益母草水苏碱生物合成影响的生理机制研究[J]. 中国中药杂志, 2022, 47(20): 5502-5507. [Zhang Y, Cui XP, Wang WQ, et al. Effects of pH value on stachydrine biosynthesis of hydroponic Leonurus japonicus and its physiological mechanism[J]. China Journal of Chinese Materia Medica, 2022, 47(20): 5502-5507.] DOI: 10.19540/j.cnki.cjcmm.20220712.101.

39.王乙晴. 基于网络药理学探讨水苏碱抗氧化应激作用[D]. 长春: 吉林大学, 2022. [Wang YQ. Based on network pharmacology to explore antioxidant stress effect of stachydrine[D]. Changchun: Jilin University, 2022.] DOI: 10.27162/d.cnki.gjlin.2022.001290.

40.Zhou F, Liu F, Liu J, et al. Stachydrine promotes angiogenesis by regulating the VEGFR2/MEK/ERK and mitochondrial-mediated apoptosis signaling pathways in human umbilical vein endothelial cells[J]. Biomed Pharmacother, 2020, 131: 110724. DOI: 10.1016/j.biopha. 2020.110724.

41.孙霁寒, 王兆丹, 孙桂菊, 等. 木犀草素对高血脂症SD大鼠肝脏脂肪变性及抗氧化水平的影响[J]. 食品工业科技, 2019, 40(11): 308-312, 317. [Sun JX, Wang ZD, Sun GJ, et al. Effect of luteolin on liver fatty degeneration and antioxidation in hyperlipemia SD rats[J]. Science and Technology of Food Industry, 2019, 40(11): 308-312, 317.] DOI: 10.13386/j.issn1002-0306.2019.11.051.

Popular papers
Last 6 months