Email Alerts
RSS
Volume 38 Issue 7
Jul.  2022
Turn off MathJax
Article Contents
Abstract
References
Article Navigation >  CHINESE JOURNAL OF BURNS AND WOUNDS  > 2022  >  38(7): 667-676
Fan FX,Li PT,Xia ZG,et al.Effects and molecular mechanism of exogenous L-carnitine on excessive endoplasmic reticulum stress-mediated hepatic pyroptosis in severely scald rats[J].Chin J Burns Wounds,2022,38(7):667-676.DOI: 10.3760/cma.j.cn501225-20220120-00010.
Citation: Fan FX,Li PT,Xia ZG,et al.Effects and molecular mechanism of exogenous L-carnitine on excessive endoplasmic reticulum stress-mediated hepatic pyroptosis in severely scald rats[J].Chin J Burns Wounds,2022,38(7):667-676.DOI: 10.3760/cma.j.cn501225-20220120-00010.
shu

Effects and molecular mechanism of exogenous L-carnitine on excessive endoplasmic reticulum stress-mediated hepatic pyroptosis in severely scald rats

doi: 10.3760/cma.j.cn501225-20220120-00010
  • 1.

    Department of Burn Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China

  • 2.

    Department of Plastic Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China

  • 3.

    Department of Burns and Plastic Surgery, the Fourth Affiliated Hospital of Anhui Medical University, Hefei 230022, China

  • 4.

    Department of Immunology, School of Basic Medicine, Anhui Medical University, Hefei 230032, China

Funds:

Key Science and Technology Project in Anhui Province of China 1604a0802083

More Information
    Abstract
  •   Objective  To investigate the effects and molecular mechanism of exogenous L-carnitine on hepatic pyroptosis mediated by excessive endoplasmic reticulum stress in severely scald rats.  Methods  The experimental research method was adopted. According to the random number table (the same group method below), fifteen female Sprague Dawley rats aged 6-8 weeks were divided into sham-injury group, scald alone group, and scald+carnitine group (with 5 rats in each group), and full-thickness scald of 30% total body surface area were made on the back of rats in scald alone group and scald+carnitine group, and rats in scald+carnitine group were additionally given intraperitoneal injection of L-carnitine. At post injury hour (PIH) 72, The levels of aspartate aminotransferase (AST) and alanine dehydrogenase (ALT) of biochemical indicators of liver injury were detected by automatic biochemical analyzer with the sample number of 5. At PIH 72, liver tissue damage was detected by hematoxylin-eosin staining. At PIH 72, The mRNA levels of nucleotide-binding oligomerization domain-containing protein-like receptor family pyrin domain containing 3 (NLRP3), cysteine aspartic acid specific protease 1 (caspase-1), gasderminD (GSDMD), and interleukin 1β(IL-1β) in liver tissue as pyroptosis-related markers and glucose regulatory protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in liver tissue as endoplasmic reticulum stress-related markers were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-qPCR). Protein expression levels of GRP78, CHOP, NLRP3, caspase-1, caspase-1/p20, GSDMD-N, and cleaved IL-1β in liver tissue were detected by Western blotting, and the sample numbers were all 5. HepG2 cells as human liver cancer cells were divided into dimethyl sulfoxide (DMSO) group, 0.1 μmol/L tunicamycin (TM) group, 0.2 μmol/L TM group, 0.4 μmol/L TM group, and 0.8 μmol/L TM group and were treated accordingly. After 24 h of culture, cell viability was detected by cell counting kit 8, and the intervention concentration of TM was screened, and the sample number was 5. HepG2 cells were divided into DMSO group, TM alone group, and TM+carnitine group, and treated accordingly. After 24 h of culture, the protein expression levels of GRP78, CHOP, NLRP3, caspase-1, caspase-1/p20, GSDMD-N, and cleaved IL-1β in cells were detected by Western blotting, and the sample numbers were all 3. Data were statistically analyzed with one-way analysis of variance and least significant difference-t test.  Results  At PIH 72, the AST and ALT levels of serum in scald alone group were (640±22) and (157±8) U/L, which were significantly higher than (106±13) and (42±6) U/L in sham-injury group, respectively, with t values of -46.78 and -25.98, respectively, P<0.01. The AST and ALT levels of serum in scald+carnitine group were (519±50) and (121±10) U/L, which were significantly lower than those in scald alone group, respectively, with t values of 4.93 and 6.06, respectively, P<0.01. At PIH 72, the morphology of liver tissue of rats in sham-injury group were basically normal with no obvious inflammatory cell infiltration; compared with those in sham-injury group, the liver tissue of rats in scald alone group showed a large number of inflammatory cell infiltration and disturbed cell arrangement; compared with that in scald alone group, the liver tissue of rats in scald+carnitine group showed a small amount of inflammatory cell infiltration. At PIH 72, the mRNA expression on levels of NLRP3, caspase-1, GSDMD, and IL-1β in liver tissue of rats in scald alone group were significantly higher than those in sham-injury group (with t values of 34.42, 41.93, 30.17, and 15.68, respectively, P<0.01); the mRNA levels of NLRP3, caspase-1, GSDMD, and IL-1β in liver tissue of rats in scald+carnitine group were significantly lower than those in scald alone group (with t values of 34.40, 37.20, 19.95, and 7.88, respectively, P<0.01). At PIH 72, the protein expression levels of NLRP3, caspase-1, caspase-1/p20, GSDMD-N, and cleaved IL-1β in liver tissue of rats in scald alone group were significantly higher than those in sham-injury group (with t values of 12.28, 26.92, 5.20, 10.02, and 24.78, respectively, P<0.01); compared with those in scald alone group, the protein expression levels of NLRP3, caspase-1, caspase-1/p20, GSDMD-N, and cleaved IL-1β in liver tissue of rats in scald+carnitine group were significantly decreased (with t values of 10.99, 27.96, 12.69, 8.96, and 12.27, respectively, P<0.01). At PIH 72, the mRNA levels of GRP78 and CHOP in liver tissue of rats in scald alone group were significantly higher than those in sham-injury group (with t values of 21.00 and 16.52, respectively, P<0.01), and the mRNA levels of GRP78 and CHOP in liver tissue of rats in scald+carnitine group were significantly lower than those in scald alone group (with t values of 8.92 and 8.21, respectively, P<0.01); the protein expression levels of GRP78 and CHOP in liver tissue of rats in scald alone group were significantly higher than those in sham-injury group (with t values of 22.50 and 14.29, respectively, P<0.01), and the protein expression levels of GRP78 and CHOP in liver tissue of rats in scald+carnitine group were significantly lower than those in scald alone group (with t values of 14.29 and 5.33 respectively, P<0.01). After 24 h of culture, the cell survival rates of 0.1 μmol/L TM group, 0.2 μmol/L TM group, 0.4 μmol/L TM group, and 0.8 μmol/L TM group were significantly decreased than that in DMSO group (with t values of 4.90, 9.35, 18.64, and 25.09, respectively, P<0.01). Then 0.8 μmol/L was selected as the intervention concentration of TM. After 24 h of culture, compared with that in DMSO group, the protein expression levels of GRP78 and CHOP in cells in TM alone group were significantly increased (with t values of 10.48 and 17.67, respectively, P<0.01), and the protein expression levels of GRP78 and CHOP in TM+carnitine group were significantly lower than those in TM alone group (with t values of 8.08 and 13.23, respectively, P<0.05 or P<0.01). After 24 h of culture, compared with those in DMSO group, the protein expression levels of NLRP3 and GSDMD-N in cells in TM alone group were significantly increased (with t values of 13.44 and 27.51, respectively, P<0.01), but the protein expression levels of caspase-1, caspase-1/p20, and cleaved IL-1β in cells were not significantly changed (P>0.05); compared with that in TM alone group, the protein expression levels of NLRP3 and GSDMD-N in cells in TM+carnitine group were significantly decreased (with t values of 20.49 and 21.95, respectively, P<0.01), but the protein expression levels of caspase-1, caspase-1/p20, and cleaved IL-1β in cells were not significantly changed (P>0.05).  Conclusions  In severely scald rats, exogenous L-carnitine may play a protective role against liver injury by inhibiting the pathways related to excessive endoplasmic reticulum stress-mediated pyroptosis.

     

    • FullText(HTML)
    • References(34)
  • [1]
    PorterC, TompkinsRG, FinnertyCC, et al. The metabolic stress response to burn trauma: current understanding and therapies[J]. Lancet, 2016,388(10052):1417-1426. DOI: 10.1016/S0140-6736(16)31469-6.
    [2]
    JeschkeMG, MicakRP, FinnertyCC, et al. Changes in liver function and size after a severe thermal injury[J]. Shock, 2007,28(2):172-177. DOI: 10.1097/shk.0b013e318047b9e2.
    [3]
    PriceLA, ThombsB, ChenCL, et al. Liver disease in burn injury: evidence from a national sample of 31,338 adult patients[J]. J Burns Wounds, 2007,7:e1.
    [4]
    褚万立, 柴家科, 冯永强, 等. 严重烧伤大鼠肝脏内质网应激相关蛋白的表达及其意义[J].中华医学杂志,2012,92(12):853-856. DOI: 10.3760/cma.j.issn.0376-2491.2012.12.019.
    [5]
    StanojcicM, VinaikR, AbdullahiA, et al. NLRP3 knockout enhances immune infiltration and inflammatory responses and improves survival in a burn sepsis model[J]. Immunology, 2022,165(2):195-205. DOI: 10.1111/imm.13427.
    [6]
    Al MamunA, WuY, JiaC, et al. Role of pyroptosis in liver diseases[J]. Int Immunopharmacol, 2020,84:106489. DOI: 10.1016/j.intimp.2020.106489.
    [7]
    SadigharaM, JoktajiJP, HajhashemiV, et al. Protective effects of coenzyme Q(10) and L-carnitine against statin-induced pancreatic mitochondrial toxicity in rats[J]. Res Pharm Sci, 2017,12(6):434-443. DOI: 10.4103/1735-5362.217424.
    [8]
    BusquetsS, SerpeR, ToledoM, et al. L-carnitine: an adequate supplement for a multi-targeted anti-wasting therapy in cancer[J]. Clin Nutr, 2012,31(6):889-895. DOI: 10.1016/j.clnu.2012.03.005.
    [9]
    HotaKB, HotaSK, ChaurasiaOP, et al. Acetyl-L-carnitine- mediated neuroprotection during hypoxia is attributed to ERK1/2-Nrf2-regulated mitochondrial biosynthesis[J]. Hippocampus, 2012,22(4):723-736. DOI: 10.1002/hipo.20934.
    [10]
    PatelSP, SullivanPG, LyttleTS, et al. Acetyl-L-carnitine ameliorates mitochondrial dysfunction following contusion spinal cord injury[J]. J Neurochem, 2010,114(1):291-301. DOI: 10.1111/j.1471-4159.2010.06764.x.
    [11]
    XiaZ, TianX, KongW, et al. Effects of L-carnitine on liver injury in rats and its impact on blood lipids[J]. Int J Clin Exp Med, 2018, 11(9):9768-9773.
    [12]
    LiP, XiaZ, KongW, et al. Exogenous L-carnitine ameliorates burn-induced cellular and mitochondrial injury of hepatocytes by restoring CPT1 activity[J]. Nutr Metab (Lond), 2021,18(1):65. DOI: 10.1186/s12986-021-00592-x.
    [13]
    徐晓东, 邓洋洋, 郑洪新. 糖皮质激素诱导肾虚骨质疏松症大鼠骨组织中OPG/RANKLmRAN及蛋白表达的影响[J].中华中医药学刊,2013,31(12):2623-2627.
    [14]
    中华医学会骨质疏松和骨矿盐疾病分会. 骨代谢生化标志物临床应用指南[J].中华骨质疏松和骨矿盐疾病杂志,2015,8(4):283-293. DOI: 10.3969/j.issn.1674-2591.2015.04.001.
    [15]
    苏延林, 宁斌. 骨质疏松的骨转换生物标志物及其临床应用[J/CD].转化医学电子杂志,2017,4(6):64-68. DOI: 10.3969/j.issn.2095-6894.2017.06.016.
    [16]
    NagyV, PenningerJM. The RANKL-RANK story[J]. Gerontology, 2015,61(6):534-542. DOI: 10.1159/000371845.
    [17]
    JeschkeMG, FinnertyCC, HerndonDN, et al. Severe injury is associated with insulin resistance, endoplasmic reticulum stress response, and unfolded protein response[J]. Ann Surg, 2012,255(2):370-378. DOI: 10.1097/SLA.0b013e31823e76e7.
    [18]
    RochaJ, Eduardo-FigueiraM, BarateiroA, et al. Erythropoietin reduces acute lung injury and multiple organ failure/dysfunction associated to a scald-burn inflammatory injury in the rat[J]. Inflammation, 2015,38(1):312-326. DOI: 10.1007/s10753-014-0035-7.
    [19]
    YangX, BaiH, CaiW, et al. Inhibition of Na+/H+ exchanger 1 by cariporide alleviates burn-induced multiple organ injury[J]. J Surg Res, 2013,185(2):797-804. DOI: 10.1016/j.jss.2013.06.049.
    [20]
    孔维昌, 夏正国, 田曦茜, 等. 早期补充外源性肉碱对严重烫伤大鼠肝脏线粒体损伤的影响及病理机制[J].中华烧伤杂志,2018,34(6):374-379. DOI: 10.3760/cma.j.issn.1009-2587.2018.06.012.
    [21]
    BortolottiP, FaureE, KipnisE. Inflammasomes in tissue damages and immune disorders after trauma[J]. Front Immunol, 2018,9:1900. DOI: 10.3389/fimmu.2018.01900.
    [22]
    WangZ, ZhangS, XiaoY, et al. NLRP3 inflammasome and inflammatory diseases[J]. Oxid Med Cell Longev, 2020,2020:4063562. DOI: 10.1155/2020/4063562.
    [23]
    Fernandes-AlnemriT, WuJ, YuJW, et al. The pyroptosome: a supramolecular assembly of ASC dimers mediating inflammatory cell death via caspase-1 activation[J]. Cell Death Differ, 2007,14(9):1590-1604. DOI: 10.1038/sj.cdd.4402194.
    [24]
    ShiJ, ZhaoY, WangK, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature, 2015,526(7575):660-665. DOI: 10.1038/nature15514.
    [25]
    D'SouzaCA, HeitmanJ. Dismantling the cryptococcus coat[J]. Trends Microbiol, 2001,9(3):112-113.DOI: 10.1016/s0966-842x(00)01945-4.
    [26]
    HagarJA, PowellDA, AachouiY, et al. Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock[J]. Science, 2013,341(6151):1250-1253. DOI: 10.1126/science.1240988.
    [27]
    KayagakiN, WongMT, StoweIB, et al. Noncanonical inflammasome activation by intracellular LPS independent of TLR4[J]. Science, 2013,341(6151):1246-1249. DOI: 10.1126/science.1240248.
    [28]
    ShiJ, ZhaoY, WangY, et al. Inflammatory caspases are innate immune receptors for intracellular LPS[J]. Nature, 2014,514(7521):187-192. DOI: 10.1038/nature13683.
    [29]
    SudsawardS, KhunchaiS, ThepmaleeC, et al. Endoplasmic reticulum stress, unfolded protein response and autophagy contribute to resistance to glucocorticoid treatment in human acute lymphoblastic leukaemia cells[J]. Int J Oncol, 2020,57(3):835-844. DOI: 10.3892/ijo.2020.5089.
    [30]
    NybergWA, EspinosaA. Imiquimod induces ER stress and Ca2+ influx independently of TLR7 and TLR8[J]. Biochem Biophys Res Commun, 2016,473(4):789-794. DOI: 10.1016/j.bbrc.2016.03.080.
    [31]
    JägerR, BertrandMJ, GormanAM, et al. The unfolded protein response at the crossroads of cellular life and death during endoplasmic reticulum stress[J]. Biol Cell, 2012,104(5):259-270. DOI: 10.1111/boc.201100055.
    [32]
    LeeAS. The ER chaperone and signaling regulator GRP78/BiP as a monitor of endoplasmic reticulum stress[J]. Methods, 2005,35(4):373-381. DOI: 10.1016/j.ymeth.2004.10.010.
    [33]
    QiZ, ChenL. Endoplasmic reticulum stress and autophagy[J]. Adv Exp Med Biol, 2019, 1206:167-177. DOI: 10.1007/978-981-15-0602-4_8.
    [34]
    NovoaI, ZengH, HardingHP, et al. Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2alpha[J]. J Cell Biol, 2001, 153: 1011-1022.DOI: 10.1083/jcb.153.5.1011.
    • Relative Articles

  • Relative Articles

    [1]Liu Xinzhu, Li Dawei, Jiang Min, Li Zhisheng, Feng Baigong, Shen Chuan'an. Changes in entero-insular axis function and its role in mice with severe burns[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2024, 40(7): 625-633. doi: 10.3760/cma.j.cn501225-20240520-00189
    [2]He Jiale, Dong Hongfei, Huang Xi, Zhang Yanbiao, Li Xianhui. Research advances on the role of pyroptosis in diabetic wound healing[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2024, 40(8): 785-791. doi: 10.3760/cma.j.cn501225-20230829-00068
    [3]Xie Chaoqiong, Fan Fuxiao, Li Pengtao, Cai Chen, Li Xingzhao, Song Junhui, Xu Jiegou, Xu Qinglian. Effects and mechanism of diammonium glycyrrhizinate on liver injury in severely scalded rats[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2022, 38(8): 735-743. doi: 10.3760/cma.j.cn501225-20220120-00011
    [4]Jin Xu, Wan Jia, Duan Shufang, Gong Yuzhou, Wang Fei, Chen Xulin. Role of Bruton′s tyrosine kinase in endotoxin/lipopolysaccharide-induced pyroptosis of intestinal cells in scalded mice[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2021, 37(6): 546-554. doi: 10.3760/cma.j.cn501120-20210119-00027
    [5]Tian Xixi, Kong Weichang, Li Pengtao, Xia Zhengguo, Xu Jiegou, Xu Qinglian. Effects of early supplement of exogenous L-carnitine on renal function in severely scalded rats[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2020, 36(7): 553-559. doi: 10.3760/cma.j.cn501120-20200203-00038
    [6]Kong Weichang, Xia Zhengguo, Tian Xixi, Xu Jiegou, Xu Qinglian. Effect of early supplementation of exogenous carnitine on liver mitochondrial damage in severely scalded rats and its pathological mechanism[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2018, 34(6): 374-379. doi: 10.3760/cma.j.issn.1009-2587.2018.06.012
    [8]Zhou Jiping, Gao Zhi, Sun Yexiang, Chen Xulin, Wu Xuesheng, Wang Fei. Effects of hypertonic sodium saline resuscitation on the liver damage of rats at early stage of severe scald[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2017, 33(1): 31-36. doi: 10.3760/cma.j.issn.1009-2587.2017.01.008
    [10]Liu Degui, Wang Xiaojuan, Yang Yong, Jiang Jinheng, Li Xianhui, Xue Gang. Effects of hydrogen-rich saline on liver of severely scalded rats with delayed resuscitation[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2014, 30(6): 506-511. doi: 10.3760/cma.j.issn.1009-2587.2014.06.010
    [11]CUI Fei-fei, PAN Ying-ying, DAI Yah-li, WANG Zhou- guang, XIAO Jian, JIANG Li-ping. Effects of endoplasmic reticulum stress related proteins and their mediated apoptosis in the formation of deep tissue injury of pressure ulcer in rats[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2013, 29(5): 448-453. doi: 10.3760/cma.j.issn.1009-2587.2013.05.011
    [13]LI Ying, GUO Li. Study on endoplasmic reticulum stress and injury to basic function unit of colonic motility in rats with scald injury[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2009, 25(3): 193-196. doi: 10.3760/cma.j.issn.1009-2587.2009.03.012
    [14]WANG Yan-bo, YAO Yong-ming, WANG Qiang, WANG Wen-jiang. Effect of ＂Xuebijing injection＂ on expression of high mobility group box-1 protein and acute liver injury in rats with scald injury[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2009, 25(3): 171-175. doi: 10.3760/cma.j.issn.1009-2587.2009.03.005
    [15]CHENG Tian-min, RAN Xin-ze. Studies on the treatment of combined radiation-burn injury[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2008, 24(5): 387-389.
    [16]SUN Bing-wei, CHEN Xi, CHEN Zhao-yong, Kazuhiro Katada, Gediminas Cepinskas. The inhibitory effects of extrinsic carbon monoxide-releasing molecules Ⅱ on inflammatory responses in liver ofmice with severe burns[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2007, 23(3): 179-183.
    [17]HAO Dai-feng, CHAI Jia-ke, WU Yan-qiu. Cbanges in the expression of rat bepatic lipid metabolism related genes in response to burn wound sepsis as assessed by DNA arrays[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2006, 22(4): 250-253.
    [18]Ma Xiu-ling, Guo Chang-jiang, Geng Zhan-hui, Yang Ji-jun, Wei Jing-yu, Gao Lan-xing. The regulatory effects of arginine on hepatic insulin-like growth factor-1 secretion in rats and its implication[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2005, 21(4): 255-258.
    [19]CHEN Xu-lin, XIA Zhao-fan, WEI Duo, BEN Dao-feng, WANG Yong-jie, WANG Chang-rong, DENG Nian-qing. The modulating role of p38 mitogen-activated protein kinase in the expression of tumor necrosis factor-α in hepatic cells and its role in hepatic injury in severely burned rats[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2005, 21(6): 418-421.
    [20]HAO Dai-feng, GUO Zhen-rong, CHAO Jia-ke, WU Yan-qiu. The influence of lipopolysaccharide on adipose metabolism in liver during shock stage of scalded rats[J]. CHINESE JOURNAL OF BURNS AND WOUNDS, 2005, 21(5): 333-335.
    • Supplements(0)
    • Cited By
  • Created with Highcharts 5.0.7Amount of accessChart context menuAbstract Views, HTML Views, PDF Downloads StatisticsAbstract ViewsHTML ViewsPDF Downloads2024-052024-062024-072024-082024-092024-102024-112024-122025-012025-022025-032025-0305101520
    Created with Highcharts 5.0.7Chart context menuAccess Class DistributionFULLTEXT: 27.5 %FULLTEXT: 27.5 %META: 66.0 %META: 66.0 %PDF: 6.5 %PDF: 6.5 %FULLTEXTMETAPDF
    Created with Highcharts 5.0.7Chart context menuAccess Area Distribution其他: 4.5 %其他: 4.5 %San Mateo: 0.3 %San Mateo: 0.3 %三亚: 0.3 %三亚: 0.3 %上海: 1.3 %上海: 1.3 %东莞: 0.3 %东莞: 0.3 %丽江: 2.4 %丽江: 2.4 %北京: 0.5 %北京: 0.5 %北方邦: 0.3 %北方邦: 0.3 %南京: 0.5 %南京: 0.5 %南宁: 0.3 %南宁: 0.3 %南昌: 0.8 %南昌: 0.8 %合肥: 0.5 %合肥: 0.5 %天津: 0.3 %天津: 0.3 %宣城: 0.3 %宣城: 0.3 %张家口: 4.2 %张家口: 4.2 %成都: 0.8 %成都: 0.8 %拉贾斯坦邦: 2.6 %拉贾斯坦邦: 2.6 %昆明: 0.8 %昆明: 0.8 %曼谷: 0.3 %曼谷: 0.3 %杭州: 0.3 %杭州: 0.3 %梧州: 0.5 %梧州: 0.5 %沈阳: 0.8 %沈阳: 0.8 %洛阳: 1.0 %洛阳: 1.0 %济南: 1.0 %济南: 1.0 %海得拉巴: 0.8 %海得拉巴: 0.8 %淮南: 0.8 %淮南: 0.8 %漯河: 1.0 %漯河: 1.0 %潍坊: 0.3 %潍坊: 0.3 %芒廷维尤: 59.9 %芒廷维尤: 59.9 %芝加哥: 0.3 %芝加哥: 0.3 %苏州: 1.3 %苏州: 1.3 %西宁: 2.6 %西宁: 2.6 %西安: 0.3 %西安: 0.3 %运城: 0.3 %运城: 0.3 %鄂州: 0.3 %鄂州: 0.3 %重庆: 6.8 %重庆: 6.8 %长沙: 0.5 %长沙: 0.5 %青岛: 0.3 %青岛: 0.3 %其他San Mateo三亚上海东莞丽江北京北方邦南京南宁南昌合肥天津宣城张家口成都拉贾斯坦邦昆明曼谷杭州梧州沈阳洛阳济南海得拉巴淮南漯河潍坊芒廷维尤芝加哥苏州西宁西安运城鄂州重庆长沙青岛

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(7)  / Tables(2)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (251) PDF downloads(25) Cited by()
    Proportional views
    Related

    Copyright © Chinese Journal of Burns京ICP备07035254号-14

    E-mail：shaoshangzazhi@163.com

    Website：https://zhsszz.xml-journal.net/

    Supported by: Beijing Renhe Information Technology Co. Ltd    

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return