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烫伤大鼠腹腔巨噬细胞释放细胞因子作用的研究 [Abstract] Thepurposeofthisstudyistoinvestigatethereleaseofcytokinesbyperitonealmacrophagesinratsafterburninjury.Inthisstudy,weexploredthechangesinthecytokinelevelsintheperitonealmacrophagesofratsafterburninjury,inordertoprovideatheoreticalbasisforthestudyofburninjuryandassociatedimmuneresponses. [Keywords] Burninjury,peritonealmacrophages,cytokines [Background] Burninjuryisacommontypeoftraumathatcanleadtosignificanttissuedamageandsystemicinflammatoryresponsesyndrome(SIRS).Peritonealmacrophagesplayacriticalroleintheimmuneresponsetoburninjury,releasingcytokineswhichcanleadtoinflammationandimmunesystemactivation.Previousstudieshaveshownthatthecytokinelevelsareelevatedintheperipheralbloodofburnpatients,butthemechanismsunderlyingthesechangesremainunclear. [Methods] MaleWistarratsweighing220-250gwererandomlydividedintoacontrolgroupandaburninjurygroup(n=10each).Theburninjurygroupwassubjectedtoa30%totalbodysurfacearea(TBSA)scaldburnthroughhotwaterimmersionoftherats'shavedbacksfor10s.Thecontrolgroupreceivedashamburnbyimmersioninroomtemperaturewaterfor10s.After24h,cellswerecollectedfromtheperitonealcavitybylavagewithsterilesaline.Thecellswerethenculturedinvitrofor24h.Thecytokinelevelsinthesupernatantweremeasuredusingenzyme-linkedimmunosorbentassay(ELISA).Thelevelsofcytokinesincludingtumornecrosisfactor-α(TNF-α),interleukin-1β(IL-1β),interleukin-6(IL-6),andinterleukin-10(IL-10)weremeasured. [Results] Comparedtothecontrolgroup,thelevelsofTNF-α,IL-1β,andIL-6weresignificantlyincreasedintheperitonealmacrophagesofratsafterburninjury(p<0.01).Meanwhile,thelevelofIL-10wassignificantlydecreased(p<0.05).Theseresultsindicatethatburninjuryleadstoaninflammatoryresponseintheperitonealmacrophagesofrats,withincreasedproductionofpro-inflammatorycytokinesanddecreasedproductionofanti-inflammatorycytokines. [Conclusion] Inconclusion,ourstudydemonstratesthatburninjuryinduceschangesincytokinelevelsinperitonealmacrophagesinrats,resultinginaninflammatoryresponsewithincreasedpro

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