Email Alerts
RSS
Volume 39 Issue 5
May  2023
Turn off MathJax
Article Contents
Article Navigation >  CHINESE JOURNAL OF BURNS AND WOUNDS  > 2023  >  39(5): 424-433
Luo P,Zhang BH,Sun JC,et al.Study on the mechanism of early pancreatic exocrine function changes in severely scalded rats[J].Chin J Burns Wounds,2023,39(5):424-433.DOI: 10.3760/cma.j.cn501225-20230216-00051.
Citation: Luo P,Zhang BH,Sun JC,et al.Study on the mechanism of early pancreatic exocrine function changes in severely scalded rats[J].Chin J Burns Wounds,2023,39(5):424-433.DOI: 10.3760/cma.j.cn501225-20230216-00051.
shu

Study on the mechanism of early pancreatic exocrine function changes in severely scalded rats

doi: 10.3760/cma.j.cn501225-20230216-00051

  • Department of Burns and Plastic Surgery, the Fourth Medical Center of PLA General Hospital, Beijing 100048, China

Funds:

General Program of National Natural Science Foundation of China 82072169, 82272279

Military Logistics Scientific Research Project Health Special Project 22BJZ35

Major Program of Military Logistics Research Plan ALB18J001

More Information
    Abstract
  •   Objective   To explore the mechanism of early pancreatic exocrine function changes in severely scalded rats.   Methods   The experimental research methods was used. Eighty male Sprague-Dawley rats aged 7-8 weeks were divided into simple sham injury group ( n=8), sham injury+cholecystokinin octapeptide (CCK8) group ( n=8), severe scald+CCK8 group ( n=32), and extremely severe scald+CCK8 group ( n=32) by the random number table, which were treated accordingly. Immediately after injury of rats in the 2 sham injury groups and 1, 2, 3, and 7 days after injury of rats in the 2 scald groups, the improved methods including pancreatic duct puncture and catheterization were used to dynamically collect the pancreatic-bile juice (PBJ) of rats. The PBJ secretory volume within 1 h was recorded, and the content of pancreatic lipase, α-amylase, and trypsin in PBJ was detected by enzyme-linked immunosorbent assay (ELISA), and the number of samples was 8. The femoral venous blood was collected, and the concentrations of pancreatic lipase and α-amylase in serum were detected by standard colorimetry to reflect their activity ( n=8). The pancreatic tissue was extracted, and the levels of interleukin-1β (IL-1β) and IL-6 in pancreatic tissue were detected by ELISA ( n=8), the expression of hypoxia-inducible factor 1α (HIF-1α) in pancreatic tissue was detected by immunofluorescence method, and the histopathological changes in pancreatic tissue were observed by hematoxylin-eosin staining, the severity of pancreatic tissue injury in the 2 scald groups was evaluated by modified Schmidt method ( n=6), and the ultrastructure of acinar cells in pancreatic tissue was observed by transmission electron microscopy. Data were statistically analyzed with analysis of variance for factorial design, Tukey test, independent sample t test, and least significant difference test.   Results   Compared with the PBJ secretory volume (0.740±0.030) mL in the pancreatic tissue of rats in simple sham injury group within 1 h immediately after injury, the (0.823±0.033) mL in sham injury+CCK8 group was significantly increased ( t=4.92, P<0.05). Compared with that of rats in sham injury+CCK8 group immediately after injury, the PBJ secretory volume of rats within 1 h in severe scald+CCK8 group ((0.681±0.024), (0.608±0.056), (0.525±0.025), and (0.720±0.044) mL) and extremely severe scald+CCK8 group ((0.540±0.025), (0.406±0.021), (0.475±0.036), and (0.690±0.018) mL) was significantly decreased on 1, 2, 3, and 7 days after injury ( P<0.05). Compared with that in severe scald+CCK8 group, the PBJ secretory volume of rats within 1 h in extremely severe scald+CCK8 group was significantly decreased on 1 and 2 days after injury ( P<0.05). Compared with that of rats in simple sham injury group immediately after injury, the content of pancreatic lipase, α-amylase, and trypsin in PBJ of rats in sham injury+CCK8 group immediately after injury was significantly increased (with t values of 4.56, 3.30, and 4.99, respectively, P<0.05). Compared with that of rats in sham injury+CCK8 group immediately after injury, the content of pancreatic lipase and α-amylase in PBJ of rats in severe scald+CCK8 group and extremely severe scald+CCK8 group was significantly decreased on 1, 2, 3, and 7 days after injury ( P<0.05), the trypsin content in PBJ of rats in extremely severe scald+CCK8 group was significantly decreased on 2 days after injury ( P<0.05). Compared with that in severe scald+CCK8 group, the content of pancreatic lipase in PBJ of rats in extremely severe scald+CCK8 group was significantly decreased on 1, 2, and 3 days after injury ( P<0.05), and the content of α-amylase and trypsin in PBJ was significantly decreased on 1 and 2 days after injury ( P<0.05). There were no statistically significant differences in the activities of pancreatic lipase and α-amylase in serum of rats among the 4 groups at various time points after injury ( P>0.05). Compared with that of rats in sham injury+CCK8 group immediately after injury, the levels of IL-1β in pancreatic tissue of rats in severe scald+CCK8 group on 1, 2, and 3 days after injury and in extremely severe scald+CCK8 group on 1, 2, 3, and 7 days after injury were significantly increased ( P<0.05), and the levels of IL-6 in pancreatic tissue of rats in severe scald+CCK8 group and extremely severe scald+CCK8 group were significantly increased on 1, 2, 3, and 7 days after injury ( P<0.05). Compared with that in severe scald+CCK8 group, the IL-1β level in pancreatic tissue of rats in extremely severe scald+CCK8 group was significantly increased on 2 and 3 days after injury ( P<0.05), and IL-6 level in pancreatic tissue was significantly increased on 2 days after injury ( P<0.05). The expression levels of HIF-1α in pancreatic tissue of rats in simple sham injury group and sham injury+CCK8 group immediately after injury were lower; and compared with that in sham injury+CCK8 group immediately after injury, the expression levels of HIF-1α in pancreatic tissue of rats in the 2 scald groups increased to a certain extent at different time points after injury, and the expression position was transited from the edge of the pancreatic tissue to the whole pancreas, the expression levels of HIF-1α in pancreatic tissue of rats in the 2 scald groups tended to be normal on 7 days after injury. Compared with that in simple sham injury group immediately after injury, the proportion of acinar cell cytoplasm in pancreatic tissue of rats in sham injury+CCK8 group was increased; and with the increase of time after injury, edema, hemorrhage, necrosis, and inflammatory infiltration appeared in pancreatic tissue of rats in the 2 scald groups. Compared with that in severe scald+CCK8 group, the scores of edema, inflammatory cell infiltration, bleeding, and necrosis in pancreatic tissue of rats in extremely severe scald+CCK8 group were increased to varying degrees at various time points after injury, and the scores of pancreatic tissue of rats in the 2 scald groups basically recovered to normal on 7 days after injury. Compared with that in simple sham injury group immediately after injury, the number of enzyme granules in acinar cells of pancreatic tissue of rats in sham injury+CCK8 group was increased, and with the increase of time after injury, the enzyme granules in acinar cells of rats in the 2 scald groups were gradually reduced basically.   Conclusions   The exocrine functions of pancreas, such as synthesis and secretion of pancreatic enzymes, are decreased in the early stage in severely scalded rats. And the greater the scalded area, the more significant the decline of pancreatic exocrine function. This change may be related to hypoxic injury and inflammation in pancreatic tissue after severe scald.

     

    • FullText(HTML)
  • loading
    • References(30)
  • [1]
    Dominguez-MuñozJE. Diagnosis and treatment of pancreatic exocrine insufficiency[J]. Curr Opin Gastroenterol, 2018,34(5):349-354. DOI: 10.1097/MOG.0000000000000459.
    [2]
    ISBI Practice Guidelines Committee, SubcommitteeSteering, SubcommitteeAdvisory. ISBI practice guidelines for burn care[J]. Burns, 2016, 42(5):953-1021. DOI: 10.1016/j.burns.2016.05.013.
    [3]
    ISBI Practice Guidelines Committee, SubcommitteeAdvisory, SubcommitteeSteering. ISBI practice guidelines for burn care, part 2[J]. Burns, 2018,44(7):1617-1706. DOI: 10.1016/j.burns.2018.09.012.
    [4]
    PuH, DoigGS, HeighesPT, et al. Early enteral nutrition reduces mortality and improves other key outcomes in patients with major burn injury: a meta-analysis of randomized controlled trials[J]. Crit Care Med, 2018,46(12):2036-2042. DOI: 10.1097/CCM.0000000000003445.
    [5]
    DurnoC, CoreyM, ZielenskiJ, et al. Genotype and phenotype correlations in patients with cystic fibrosis and pancreatitis[J]. Gastroenterology, 2002,123(6):1857-1864. DOI: 10.1053/gast.2002.37042.
    [6]
    ZhangB, SunP, ShenC, et al. Role and mechanism of PI3K/AKT/FoxO1/PDX-1 signaling pathway in functional changes of pancreatic islets in rats after severe burns[J]. Life Sci, 2020, 258(118145):1-9. DOI: 10.1016/j.lfs.2020.118145.
    [7]
    RomacJM, ShahidRA, SwainSM, et al. Piezo1 is a mechanically activated ion channel and mediates pressure induced pancreatitis[J]. Nat Commun, 2018,9(1):1715. DOI: 10.1038/s41467-018-04194-9.
    [8]
    MeiQ, DengG, HuangZ, et al. Porous COS@SiO2 nanocomposites ameliorate severe acute pancreatitis and associated lung injury by regulating the Nrf2 signaling pathway in mice[J]. Front Chem, 2020, 8(720):1-12. DOI: 10.3389/fchem.2020.00720.
    [9]
    DolaiS, LiangT, OrabiAI, et al. Pancreatitis-induced depletion of syntaxin 2 promotes autophagy and increases basolateral exocytosis[J]. Gastroenterology, 2018,154(6):1805-1821.e5. DOI: 10.1053/j.gastro.2018.01.025.
    [10]
    MajumderS, ChariST. Chronic pancreatitis[J]. Lancet, 2016, 387(10031): 1957-1966. DOI: 10.1016/S0140-6736(16)00097-0.
    [11]
    HollemansRA, HallenslebenN, MagerDJ, et al. Pancreatic exocrine insufficiency following acute pancreatitis: systematic review and study level meta-analysis[J]. Pancreatology, 2018, 18(3): 253-262. DOI: 10.1016/j.pan.2018.02.009.
    [12]
    YangX, YaoL, FuX, et al. Experimental acute pancreatitis models: history, current status, and role in translational research[J]. Front Physiol, 2020,11:614591. DOI: 10.3389/fphys.2020.614591.
    [13]
    JeschkeMG, van BaarME, ChoudhryMA, et al. Burn injury[J]. Nat Rev Dis Primers, 2020,6(1):11. DOI: 10.1038/s41572-020-0145-5.
    [14]
    BittnerEA, ShankE, WoodsonL, et al. Acute and perioperative care of the burn-injured patient[J]. Anesthesiology, 2015,122(2):448-464. DOI: 10.1097/ALN.0000000000000559.
    [15]
    AgrawalA, AlagusundarmoorthySS, JasdanwalaS. Pancreatic involvement in critically ill patients[J/OL]. J Pancreas, 2015, 16(4):346-355[2023-02-16].https://www.researchgate.net/publication/281210070_Pancreatic_Involvement_in_Critically_ill_Patients. https://www.researchgate.net/publication/281210070_Pancreatic_Involvement_in_Critically_ill_Patients
    [16]
    SalujaA, DudejaV, DawraR, et al. Early intra-acinar events in pathogenesis of pancreatitis[J]. Gastroenterology, 2019,156(7):1979-1993. DOI: 10.1053/j.gastro.2019.01.268.
    [17]
    ArvanitakisM, OckengaJ, BezmarevicM, et al. ESPEN guideline on clinical nutrition in acute and chronic pancreatitis[J]. Clin Nutr, 2020, 39(3):612-631. DOI: 10.1016/j.clnu.2020.01.004.
    [18]
    HirotaM, OhmurayaM, HashimotoD, et al. Roles of autophagy and pancreatic secretory trypsin inhibitor in trypsinogen activation in acute pancreatitis[J]. Pancreas, 2020,49(4):493-497. DOI: 10.1097/MPA.0000000000001519.
    [19]
    WilsonMD, SugdenP, DurraniA, et al. Acute pancreatitis complicating 50% full-thickness burns in a 5-year-old child[J]. Burns, 2003, 29(6):619-621. DOI: 10.1016/s0305-4179(03)00144-x.
    [20]
    OsukaA, SugenoyaS, OnishiS, et al. Acute pancreatitis and necrotizing colitis following extensive burn injury[J]. Acute Med Surg, 2016,3(3):283-285. DOI: 10.1002/ams2.181.
    [21]
    NeuhöferP, RoakeCM, KimSJ, et al. Acinar cell clonal expansion in pancreas homeostasis and carcinogenesis[J]. Nature, 2021,597(7878):715-719. DOI: 10.1038/s41586-021-03916-2.
    [22]
    ApteMV, HaberPS, ApplegateTL, et al. Periacinar stellate shaped cells in rat pancreas: identification, isolation, and culture[J]. Gut, 1998,43(1):128-133. DOI: 10.1136/gut.43.1.128.
    [23]
    CriscimannaA, SpeicherJA, HoushmandG, et al. Duct cells contribute to regeneration of endocrine and acinar cells following pancreatic damage in adult mice[J]. Gastroenterology, 2011,141(4):1451-1462, 1462.e1-e6. DOI: 10.1053/j.gastro.2011.07.003.
    [24]
    ZhouQ, MeltonDA. Pancreas regeneration[J]. Nature, 2018,557(7705):351-358. DOI: 10.1038/s41586-018-0088-0.
    [25]
    JiZ, LuM, XieH, et al. β cell regeneration and novel strategies for treatment of diabetes (review)[J]. Biomed Rep, 2022,17(3):72. DOI: 10.3892/br.2022.1555.
    [26]
    GaoL, LuGT, LuYY, et al. Diabetes aggravates acute pancreatitis possibly via activation of NLRP3 inflammasome in db/db mice[J]. Am J Transl Res, 2018, 10(7):2015-2025.
    [27]
    TybergA, KariaK, GabrM, et al. Management of pancreatic fluid collections: a comprehensive review of the literature[J]. World J Gastroenterol, 2016,22(7):2256-2270. DOI: 10.3748/wjg.v22.i7.2256.
    [28]
    WangCC, GrossmanMI. Physiological determination of release of secretin and pancreozymin from intestine of dogs with transplanted pancreas[J]. Am J Physiol, 1951,164(2):527-545. DOI: 10.1152/ajplegacy.1951.164.2.527.
    [29]
    MirzaKB, AlendaA, EftekharA, et al. Influence of Cholecystokinin-8 on compound nerve action potentials from ventral gastric vagus in rats[J]. Int J Neural Syst, 2018, 28(9):1850006. DOI: 10.1142/S0129065718500065.
    [30]
    TandayN, EnglishA, LaffertyRA, et al. Benefits of sustained upregulated unimolecular GLP-1 and CCK receptor signalling in obesity-diabetes[J]. Front Endocrinol (Lausanne), 2021, 12(674704):1-13. DOI: 10.3389/fendo.2021.674704.
    • Relative Articles
    • Supplements(0)
    • Cited By
  • 加载中

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(6)  / Tables(1)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (1651) PDF downloads(28) 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