Деструктивный панкреатит: механизмы гибели клетки и их возможное клиническое значение
- Авторы: Фирсова В.1, Паршиков В.1
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Учреждения:
- Нижегородская государственная медицинская академия, Нижний Новгород, Российская Федерация
- Выпуск: Том 6, № 1 (2013)
- Страницы: 100-106
- Раздел: Оригинальные статьи
- URL: https://vestnik-surgery.com/journal/article/view/170
- DOI: https://doi.org/10.18499/2070-478X-2013-6-1-100-106
- ID: 170
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Аннотация
В обзоре рассмотрены основные механизмы гибели клетки при остром панкреатите. Подробно анализированы варианты апоптоза и фазы его развития. Отражено значение рецепторных комплексов, инициирующих смерть клетки, роль каспаз и других ключевых структур молекулярного уровня. Дана оценка соотношению некроза и апоптоза в течении деструктивного панкреатита, зависимости указанных процессов от ряда интрацеллюлярных и внеклеточных сигналов, уровня макроэргов, экспрессии регуляторных белков. Подчеркнуто протективное значение каспазного каскада реакций в отношении некроза клетки. Приведены данные, указывающие на негативное прогностическое значение некроза как типа гибели клетки и обратное в отношении апоптоза. Представлены особенности аутофагии и ее вариантов, описаны морфологические признаки. На основании анализа публикаций авторы делают вывод о том, что процессы, ответственные за гибель клеток, многокомпонентны, имеют различные уровни регуляции и в ряде случаев связаны между собой общими факторами молекулярного уровня. Разработка методов терапии, направленных на блокирование какого-либо одного механизма может не привести к желаемому эффекту. Имеют определенные перспективы исследования, направленные на изменение экспрессии генов, участвующих в каскаде реакций воспаления, апоптоза, некроза.
Ключевые слова
Об авторах
В.Г. Фирсова
Нижегородская государственная медицинская академия, Нижний Новгород, Российская Федерация
Автор, ответственный за переписку.
Email: author@vestnik-surgery.com
врач – хирург городской больницы №35, г. Нижний Новгород
В.В. Паршиков
Нижегородская государственная медицинская академия, Нижний Новгород, Российская Федерация
Email: author@vestnik-surgery.com
д.м.н., профессор кафедры госпитальной хирургии им. Б.А.Королева Нижегородской государственной медицинской академии
Список литературы
- Gordeeva a.V., Labas iu.a., Zviagil'skaia r.a. apoptoz odnokletochnyh organizmov: mekhanizmy i ehvolyuciya. [apoptosis of single-celled organisms: mechanisms and evolution]. Biokhimiia, 2004; 10(69): 1301-1313. - (in russian).
- Gostishchev V.k., khrupkin V.i., afanas'ev a.N. i dr. Lechebno-diagnosticheskaya taktika pri ostrom destruktivnom pankreatite v zavisimosti ot proizvoditel'nosti integral'nyh shkal tyazhesti. [Medical-diagnostic tactics in acute destructive pancreatitis depending on the performance of integrated scales of severity]. Materialy VII Vserossiiskoi konferencii obshchikh khirurgov s mezhdunarodnym uchastiem [Proc. 7th allrussian conference of general surgeons with international participation]. krasnoiarsk, 2012; 66-71. - (in russian).
- savel'ev V.s., Filimonov M.i., Burnevich s.Z. Pankreonekrozy [Necrotizing pancreatitis]. Moscow,
- Meditsinskoe informatsionnoe agentstvo, 2008; 264 p. - (in russian).
- Tolstoi a.D. Ostryi pankreatit. Trudnosti, vozmozhnosti, perspektivy. Klinicheskie lektsii [acute pancreatitis. Difficulties, opportunities and prospects]. saint-Petersburg. Predpriiatie sPb soiuza khudozhnikov, 1997; 140 p. - (in russian).
- Banks r.a., Martin L. Freeman M.L. Prakticheskie rekomendacii pri ostrom pankreatite. [Practice guidelines in acute pancreatitis]. Am. J. Gastroenterol., 2006; 101: 2379–2400.
- Bhatia M. apoptoz pankreaticheskih acinarnyh kletok pri ostrom pankreatite: ehto horosho ili ploho? [apoptosis of pancreatic acinar cells in acute pancreatitis: is it good or bad]? J. Cell. Mol. Med., 2004; 8(3): 402-409.
- Bhatia M. apoptoz protiv nekroza pri ostrom pankreatite. [apoptosis versus necrosis in acute pancreatitis]. Am. J. Physiol. Gastrointest. Liver Physiol., 2004; 286(2): 189-196.
- Bradley E.L. sistemy klinicheski na osnove klassifikacii ostrogo pankreatita. rezyume mezhdunarodnogo simpoziuma po ostromu pankreatit. [a clinically based classification system for acute pancreatitis. summary of the international symposium on acute pancreatitis]. (atlanta, 1992). Arch. Surg., 1993; 128: 586–590.
- Chan F.k., shisler J., Bixby J.G. et al. rol' nekroza opuholi, receptor-2 faktora i receptor-vzaimodejstvuyushchego belka v zaprogrammirovannyj nekroz i protivovirusnyh otvetov. [a role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses]. J. Biol. Chem., 2003; 278(51): 51613-51621.
- Cohen G.M. Kaspazy: karateli apoptoza. [Caspases: the executioners of apoptosis]. Biochem. J., 1997; 326: 1-16.
- Criddle D.N., Gerasimenko J.V., Baumgartner h.k. et al. Signalizaciya kal'ciya i podzheludochnoj kletochnaya smert': apoptoz ili nekroz? [Calcium signalling and pancreatic cell death: apoptosis or necrosis]? Cell Death Differ., 2007; 14(7): 1285-1294.
- Czaja M.J. Funkcii autofagii v pecheni i podzheludochnoj fiziologii i boleznej. [Functions of autophagy in hepatic and pancreatic physiology and disease]. Gastroenterology, 2011; 140(7): 1895-1908.
- Danial N.N., korsmeyer s.J. Smert' kletki: kriticheskie kontrol'nye tochki. [Cell death: critical control points]. Cell, 2004; 116(2): 205-19.
- Edinger a.L., Thompson C.B. Smert' po dizajnu: apoptoza, nekroza i autofagii. [Death by design: apoptosis, necrosis and autophagy]. Curr. Opin. Cell Biol., 2004; 16(6): 663-669.
- Feng D., Park o., radaeva s. et al. interlejkin-22 uluchshaet "cerulein"-inducirovannogo pankreatita u myshej putem ingibirovaniya puti autofagii. [interleukin-22 ameliorates cerulein-induced pancreatitis in mice by inhibiting the autophagic pathway]. Int. J. Biol. Sci., 2012; 8(2): 249-257.
- Festjens N., Vanden Berghe T., Vandenabeele P. Necrosis, horosho srezhissirovannyj forma kletochnoj gibeli: signal'nye kaskady, vazhnyh posrednikov i soputstvuyushchej immunnyj otvet. [a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response]. Biochim, Biophys. Acta., 2006; 1757(9-10): 1371-1387.
- Fortunato F., Deng X., Gates L.k. et al. Pankreaticheskij otvet na ehndotoksin posle hronicheskogo vozdejstviya alkogolya: perekhodit' ot apoptoza k nekrozu. [Pancreatic response to endotoxin after chronic alcohol exposure: switch from apoptosis to necrosis]? Am. J. Physiol. Gastrointest. Liver Physiol., 2006; 290(2): 232-241.
- Gukovskaya a.s., Gukovsky i., Jung Y. et al. Holecistokinin vyzyvaet aktivaciyu kaspaz i mitohondrial'noj disfunkcii v pankreaticheskih acinarnyh kletok. roli v processah povrezhdeniya kletok pankreatita.[Cholecystokinin induces caspase activation and mitochondrial dysfunction in pancreatic acinar cells. roles in cell injury processes of pancreatitis]. J. Biol. Chem., 2002; 277(25): 22595-22604.
- Gukovskaya a.s., Pandol s.J. Puti gibeli kletok pri pankreatite i rake podzheludochnoj zhelezy. [Cell death pathways in pancreatitis and pancreatic cancer]. Pancreatology, 2004; 4(6): 567-86.
- Gukovskaya a.s., Perkins P., Zaninovic V. et al. Mekhanizmy kletochnoj gibeli posle zakuporki protoka podzheludochnoj zhelezy v opossumov i krys. [Mechanisms of cell death after pancreatic duct obstruction in the opossum and the rat]. Gastroenterology, 1996; 110(3): 875-884.
- Gukovsky i., Pandol s.J., Gukovskaya a.s. organelly disfunkcii v patogeneze pankreatita. antioksid. [organellar dysfunction in the pathogenesis of pancreatitis. Antioxid]. Redox Signal., 2011; 15(10): 2699-2710.
- Gupta s. Faktor-Al'fa-inducirovannogo nekroza opuholi apoptoz T-kletok ot vozrasta cheloveka: rol' TNFr-I i nizhelezhashchih signal'nyh molekul. [Tumor necrosis factor-alpha-induced apoptosis in T cells from aged humans: a role of TNFr-i and downstream signaling molecules]. Exp. Gerontol., 2002; 37(2-3): 93-99.
- hashimoto D., ohmuraya M., hirota M. et al. uchastie autofagii v aktivacii tripsinogena v podzheludochnoj acinusa kletki. [involvement of autophagy in trypsinogen activation within the pancreatic acinar cells]. J. Cell Biol., 2008; 181 (7): 1065-1072.
- he s., Wang L., Miao L. et al. vzaimodejstvie receptornogo belka kinazy-3 opredelyaet nekroticheskie reakcii kletochnogo TNFalpha. [receptor interacting protein kinase-3 determines cellular necrotic response to TNFalpha]. Cell, 2009; 137(6): 1100-1111.
- henriquez M., armisén r., stutzin a., Quest a.F. Gibel' kletok putem nekroza, reguliruemoj put'. [Cell death by necrosis, a regulated way to go]. Curr. Mol. Med., 2008; 8(3): 187-206.
- ishidoh k., kominami E. Obrabotka i aktivaciya lizosomal'nyh proteinaz. [Processing and activation of lysosomal proteinases]. Biol. Chem., 2002; 383(12): 18271831.
- izyumov D.s., avetisyan a.V., Pletjushkina o.Y. et al. «Plata za strah»: tranzitornaya trekhkratnoe snizhenie vnutrikletochnogo aTP urovnya nakladyvaet apoptoza. [«Wages of fear»: transient threefold decrease in intracellular aTPlevel imposes apoptosis]. Biochim. Biophys. Acta., 2004; 1658(1-2): 141-147.
- kaiser a.M., saluja a.k., sengupta a. et al. vzaimosvyaz' mezhdu tyazhest'yu, nekroza i apoptoza v pyati modelyah ehksperimental'nogo ostrogo pankreatita. [relationship between severity, necrosis, and apoptosis in five models of experimental acute pancreatitis]. Am. J. Physiol., 1995; 269(5 Pt 1): 1295-1304.
- kroemer G., Marino G., Levine B. autofagiya i kompleksnaya reakciya na stress. [autophagy and the integrated stress response]. Mol. Cell., 2010; 40(2): 280-293.
- Li P., Nijhawan D., Budihardjo i. et al. Citohroma S i daTP-zavisimogo formirovaniya apaf-1/kaspaza-9 kompleks iniciiruet apoptoticheskoj proteazy kaskada. [Cytochrome c and daTP-dependent formation of apaf-1/caspase-9 complex initiates an apoptotic protease cascade]. Cell, 1997; 91(4): 479-489.
- Lü C.X., Fan T.J., hu G.B., Cong r.s. apoptoz-induciruyushchih faktorov i apoptoza. [apoptosis-inducing factor and apoptosis]. Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai), 2003; 35(10): 881-885.
- Mahajan U.M., Gupta C., Wagh P.r. et al. izmeneniya pri vospalitel'nyh/apoptoznogo puti i modifikacii gistonov na "nordihydroguaiaretic" kislota predotvrashchaet ostrogo pankreatita v shvejcarskih belyh besporodnyh myshej. [alteration in inflammatory/apoptotic pathway and histone modifications by nordihydroguaiaretic acid prevents acute pancreatitis in swiss albino mice]. Apoptosis, 2011; 16(11):1138-1149. 33. Maiuri M.C., Zalckvar E., kimchi a., kroemer G. selfeating and self-killing: crosstalk between autophagy and apoptosis. Nat. Rev. Mol. Cell Biol., 2007; 8(9): 741-752.
- Mareninova o.a., hermann k., French s.W. et al. narusheniya autofagii potok posrednichaet acinarnoj obrazovanie vakuolej kletok i aktivaciya tripsinogena v modelyah gryzunov ostrogo pankreatita. [impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis]. J. Clin. Invest., 2009; 119(11): 3340–3355.
- Mareninova o.a., sung k.F., hong P. et al. Gibel' kletok pri pankreatite: kaspaz zashchity ot pankreonekroza. [Cell death in pancreatitis: caspases protect from necrotizing pancreatitis]. J. Biol. Chem., 2006; 281(6): 3370-3381.
- Mizuno T., Zhong X., rothstein T.L. FAS-oposredovannyj apoptoz v kletkah B. [Fas-induced apoptosis in B cells]. Apoptosis, 2003; 8(5): 451-460.
- Mizushima N., Levine B., Cuervo a.M., klionsky D.J. autofagiya boretsya s bolezn'yu posredstvom sotovoj svyazi samoperevarivaniya.[autophagy fights disease through cellular self-digestion]. Nature, 2008; 451: 1069–1075.
- Moquin D., Chan F.k. Molekulyarnaya regulyaciya zaprogrammirovannoj nekroticheskie povrezhdeniya kletok. [The molecular regulation of programmed necrotic cell injury]. Trends Biochem Sci., 2010; 35(8): 434-441.
- Moretti L., Cha Y.i., Niermann k.J., Lu B. pereklyuchenie mezhdu apoptoza i autofagii: radiacionno-inducirovannyh ehndoplazmaticheskij retikulum stress? [switch between apoptosis and autophagy: radiation-induced endoplasmic reticulum stress]? Cell Cycle, 2007; 6(7): 793-798.
- Nakamura Y., Do J.h., Yuan J. et al. vospalitel'nyh kletok, reguliruyushchih r53 i kaspazy pri ostrom pankreatite. [inflammatory cells regulate p53 and caspases in acute pancreatitis]. Am. J. Physiol. Gastrointest. Liver Physiol., 2010; 298(1): 92-100.
- Niederau C., Grendell J.h. vnutrikletochnye vakuoli pri ehksperimental'nom ostrom pankreatite u krys i myshej podkislennoj otseka. [intracellular vacuoles in experimental acute pancreatitis in rats and mice are an acidified compartment]. J. Clin. Invest., 1988; 81: 229–236.
- Nixon r.a., Yang D.s., Lee J.h. Lizosomal'nyh nejrodegenerativnyh rasstrojstv: kontinuum ot razvitiya v pozdnem vozraste.[Neurodegenerative lysosomal disorders: a continuum from development to late age]. Autophagy, 2008; 4(5): 590-599.
- orlichenko L., stolz D.B., Noel P. et al. ADF-ribozilirovaniya faktora 1 belok reguliruet aktivaciyu tripsinogena cherez torgovlyu organell iz prokacepsina B belka i sozrevanie autofagii pri ostrom pankreatite. [aDP-ribosylation factor 1 protein regulates trypsinogen activation via organellar trafficking of procathepsin B protein and autophagic maturation in acute pancreatitis]. J. Biol. Chem., 2012; 287 (29): 24284-24293.
- Padanilam B.J. Kletochnoj smerti, vyzvannoj ostroj pochechnoj travmatizma: perspektivy na vklad apoptoza i nekroza. [Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis]. Am. J. Physiol. Renal Physiol., 2003; 284(4): 608-627.
- Pandol s.J., Poucell-hatton s. Mekhanizmy kletochnoj gibeli posle zakuporki protoka podzheludochnoj zhelezy v opossumov i krys.[Mechanisms of cell death after pancreatic duct obstruction in the opossum and the rat]. Gastroenterology, 1996; 110(3): 875-884.
- rozengurt E. Proteinkinaza d signalizacii: neskol'ko biologicheskih funkcij v norme i patologii. [Protein kinase D signaling: multiple biological functions in health and disease]. Physiology (Bethesda), 2011; 26(1): 23-33.
- sandoval D., Gukovskaya a., reavey P. et al. Rol' nejtrofilov i trombocitov aktiviruyushchego faktora, oposredstvuyushchego v ehksperimental'nom pankreatite. [The role of neutrophils and platelet-activating factor in mediating experimental pancreatitis]. Gastroenterology, 1996; 111(4): 1081-1091.
- satoh a., Gukovskaya a.s., Nieto J.M. et al. PkC-delta and -epsilon regulate NF-kappaB activation induced by cholecystokinin and TNF-alpha in pancreatic acinar cells. Am. J. Physiol. Gastrointest. Liver Physiol., 2004; 287(3): 582-591.
- sung k.F., odinokova i.V., Mareninova o.a. et al. Pro vyzhivanie i bcl-2 belkov stabilizirovat' podzheludochnoj mitohondrii i zashchity ot nekroza pri ehksperimental'nom pankreatite. [Prosurvival Bcl-2 proteins stabilize pancreatic mitochondria and protect against necrosis in experimental pancreatitis]. Exp. Cell Res., 2009; 315(11): 1975-1989.
- Thorburn a. Receptor-inducirovannogo smerti, ubivaya kletki. [Death receptor-induced cell killing]. Cell Signal, 2004; 16(2): 139-144.
- Thrower E.C., Gorelick F.s., husainb s.Z. Molekulyarnye i kletochnye mekhanizmy travmy podzheludochnoj zhelezy. [Molecular and cellular mechanisms of pancreatic injury]. Curr. Opin. Gastroenterol., 2010; 26(5): 484–489.
- Thrower E.C., Yuan J., Usmani a., Liu Y., Jones C., Minervini s.N., alexandre M., Pandol s.J., Guha s. roman proteinkinazy ingibitor d oslablyaet nachale sobytij ehksperimental'nogo pankreatita v izolirovannyh krys acinusov. [a novel protein kinase D inhibitor attenuates early events of experimental pancreatitis in isolated rat acini]. Am. J. Physiol. Gastrointest. Liver Physiol., 2011; 300(1): 120-129.
- Vandenabeele P., Declercq W., Van herreweghe F., Vanden Berghe T. Rol' kinaz riP1 i riP3 v FNO-inducirovannogo nekroza. [The role of the kinases riP1 and riP3 in TNFinduced necrosis]. Sci. Signal, 2010; 3(115): 4.
- Vanlangenakker N., Vanden Berghe T., krysko D.V. et al. Molekulyarnye mekhanizmy i patofiziologiya nekroticheskoj gibeli kletok. [Molecular mechanisms and pathophysiology of necrotic cell death]. Curr. Mol. Med., 2008; 8(3): 207-220.
- Vercammen D., Beyaert r., Denecker G. et al. ingibirovanie kaspaz povyshaet chuvstvitel'nost' L929 kletok k nekrozu, oposredovannyj faktorom nekroza opuholi. [inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor]. J. Exp. Med., 1998; 187(9): 1477-1485.
- Vercammen D., Brouckaert G., Denecker G. et al. Dvojnoj signalizacii receptora FAS: posvyashchenie kak apoptoticheskoj i nekroticheskoj gibeli kletok putej. [Dual signaling of the Fas receptor: initiation of both apoptotic and necrotic cell death pathways]. J. Exp. Med., 1998; 188(5): 919-930.
- Voronina s.G., Barrow s.L, simpson a.W. et al. Dinamicheskie izmeneniya v citozol'noj i mitohondrial'noj urovnya ATF v pankreaticheskih acinarnyh kletok. [Dynamic changes in cytosolic and mitochondrial aTP levels in pancreatic acinar cells]. Gastroenterology, 2010; 138(5): 1976-1987.
- Wang J., Chen G., Gong h. et al. uluchshenie ehksperimental'nogo ostrogo pankreatita otvarami " Dachengqi "cherez regulirovanie nekroz-apoptoz pereklyuchatel' v pankreaticheskih acinarnyh kletok.[amelioration of experimental acute pancreatitis with Dachengqi Decoction via regulation of necrosis-apoptosis switch in the pancreatic acinar cell]. PLoS One, 2012; 7(7): 40160.
- Watanabe o., Baccino F.M., steer M.L., Meldolesi J. supra maksimal'naya stimulyaciya caerulein i ul'trastruktury acinarnyh kletok podzheludochnoj zhelezy krys: rannie morfologicheskie izmeneniya pri razvitii ehksperimental'nogo pankreatita. [supramaximal caerulein stimulation and ultrastructure of rat pancreatic acinar cell: early morphological changes during development of experimental pancreatitis]. Am. J. Physiol., 1984; 246 (4 Pt 1): 457-467.
- Weng T.i., Wu h.Y., Chen B.L., Liu s.h. honokiol oslablyaet tyazhest' ostrogo pankreatita i svyazannyh s povrezhdeniem legkih cherez uskorenie acinoznyh kletok apoptoza. [honokiol attenuates the severity of acute pancreatitis and associated lung injury via acceleration of acinar cell apoptosis]. Shock,. 2012; 37(5): 478-484.
- Xie Z., klionsky D.J. formirovanie autofagosomii: osnovnye mashiny i prisposobleniya. [autophagosome formation: core machinery and adaptations]. Nat. Cell Biol., 2007; 9(10): 1102-1109.
- Yuan J., Liu Y., Tan T. et al. Proteinkinaza D reguliruet putej smerti kletki v ehksperimental'nom pankreatite. [Protein kinase d regulates cell death pathways in experimental pancreatitis]. Front Physiol.,. 2012; 3: 60.
- Zhang D.W., shao J., Lin J. et al. riP3, ehnergeticheskij metabolizm regulyator, kotoryj pereklyuchaet FNO-inducirovannaya gibel' kletok ot apoptoza k nekrozu. [riP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis]. Science, 2009; 325(5938): 332336. recieved 16.10.2012