化濕潤燥方對干燥綜合征模型小鼠頜下腺結(jié)構(gòu)和功能的影響

化濕潤燥方對干燥綜合征模型小鼠頜下腺結(jié)構(gòu)和功能的影響化濕潤燥方對干燥綜合征模型小鼠頜下腺結(jié)構(gòu)和功能的影響

摘要：干燥綜合征是一種常見的自身免疫疾病，其中頜下腺受到嚴(yán)重影響。本研究旨在探討中藥方劑“化濕潤燥方”對干燥綜合征模型小鼠頜下腺結(jié)構(gòu)和功能的影響。實驗設(shè)計為健康對照組（健康小鼠）、模型組（干燥綜合征小鼠）和化濕潤燥方組（干燥綜合征模型小鼠接受化濕潤燥方治療）。通過觀察頜下腺組織病理學(xué)變化、免疫組織化學(xué)染色以及檢測腺體功能相關(guān)指標(biāo)，評估化濕潤燥方對于干燥綜合征模型小鼠頜下腺結(jié)構(gòu)和功能的影響。

結(jié)果顯示，與健康對照組相比，模型組小鼠頜下腺組織呈現(xiàn)明顯的病理學(xué)改變，包括腺泡萎縮、上皮細(xì)胞變性壞死以及間質(zhì)纖維化。免疫組織化學(xué)染色結(jié)果顯示，模型組小鼠頜下腺組織中細(xì)胞凋亡水平明顯增加，伴隨著減少的PAS染色陽性細(xì)胞和增加的α-干擾素（IFN-α）表達(dá)。此外，模型組小鼠頜下腺腺液分泌量明顯降低。

然而，化濕潤燥方組小鼠頜下腺組織結(jié)構(gòu)顯示明顯改善，腺泡形態(tài)恢復(fù)正常，上皮細(xì)胞壞死減少，間質(zhì)纖維化程度減輕。此外，化濕潤燥方組小鼠頜下腺組織中細(xì)胞凋亡水平明顯降低，PAS染色陽性細(xì)胞數(shù)量和IFN-α表達(dá)明顯增加，并且頜下腺腺液分泌量增加。

綜合以上結(jié)果，我們可以得出結(jié)論：化濕潤燥方對干燥綜合征模型小鼠頜下腺結(jié)構(gòu)和功能有明顯改善作用。其通過減少上皮細(xì)胞凋亡和間質(zhì)纖維化程度，增加PAS染色陽性細(xì)胞和IFN-α表達(dá)，促進(jìn)頜下腺腺液分泌。因此，化濕潤燥方具有潛在的治療干燥綜合征的藥物作用，并值得進(jìn)一步研究和開發(fā)。

關(guān)鍵詞：干燥綜合征；化濕潤燥方；頜下腺；細(xì)胞凋亡；腺液分泌。

Abstract:Sj?gren'ssyndromeisacommonautoimmunediseasethatseverelyaffectssalivaryglands,includingthesubmandibulargland.ThisstudyaimedtoinvestigatetheeffectsofthetraditionalChinesemedicineformula"HuaShiRunZhuangFang"onthestructureandfunctionofthesubmandibularglandinamousemodelofSj?gren'ssyndrome.Theexperimentaldesignincludedahealthycontrolgroup(healthymice),amodelgroup(Sj?gren'ssyndromemice),andanHuaShiRunZhuangFanggroup(Sj?gren'ssyndromemicetreatedwithHuaShiRunZhuangFang).TheeffectsofHuaShiRunZhuangFangonthestructureandfunctionofthesubmandibularglandintheSj?gren'ssyndromemodelmicewereevaluatedthroughtheobservationofhistopathologicalchangesintheglandulartissue,immunohistochemicalstaining,andmeasurementofglandularfunction-relatedindicators.

Theresultsshowedthatcomparedtothehealthycontrolgroup,thesubmandibularglandtissueofthemodelgroupmiceexhibitedsignificantpathologicalchanges,includingatrophyofacini,degenerationandnecrosisofepithelialcells,andinterstitialfibrosis.Immunohistochemicalstainingresultsshowedthatthelevelofapoptosisinthesubmandibularglandtissueofthemodelgroupmiceincreasedsignificantly,accompaniedbyadecreasednumberofPAS-positivecellsandanincreasedexpressionofalpha-interferon(IFN-α).Additionally,thesecretionofsubmandibularglandfluidwassignificantlyreducedinthemodelgroupmice.

However,thesubmandibularglandtissuestructureoftheHuaShiRunZhuangFanggroupmiceshowedsignificantimprovement,withrestorationofacinarmorphology,reducedepithelialcelldeath,andlesssevereinterstitialfibrosis.Moreover,thelevelofapoptosisinthesubmandibularglandtissueoftheHuaShiRunZhuangFanggroupmicedecreasedsignificantly,thenumberofPAS-positivecellsandIFN-αexpressionincreasedsignificantly,andsubmandibularglandfluidsecretionincreased.

Inconclusion,HuaShiRunZhuangFanghasasignificantimprovementonthestructureandfunctionofthesubmandibularglandinamousemodelofSj?gren'ssyndrome.Itachievesthisbyreducingepithelialcellapoptosisandthedegreeofinterstitialfibrosis,increasingthenumberofPAS-positivecellsandIFN-αexpression,andpromotingsubmandibularglandfluidsecretion.Therefore,HuaShiRunZhuangFanghaspotentialasatherapeuticdrugforSj?gren'ssyndromeanddeservesfurtherresearchanddevelopment.

Keywords:Sj?gren'ssyndrome;HuaShiRunZhuan