天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
11期
1103-1105
,共3页
三七%皂苷类%糖尿病视网膜病变%视网膜神经节细胞%髓磷脂蛋白质类%氧化性应激
三七%皂苷類%糖尿病視網膜病變%視網膜神經節細胞%髓燐脂蛋白質類%氧化性應激
삼칠%조감류%당뇨병시망막병변%시망막신경절세포%수린지단백질류%양화성응격
panax notoginseng%saponins%diabetic retinopathy%retinal ganglion cells%myelin proteins%oxidative stress
目的：探讨三七三醇皂苷（PTS）对糖尿病大鼠视网膜神经节细胞（RGC）的保护作用及机制。方法SD大鼠随机分为对照组、糖尿病组及治疗组，糖尿病组及治疗组腹腔注射链脲佐菌素诱导糖尿病动物模型，治疗组给予PTS 50 mg·kg-1·d-1灌胃，1个月后免疫荧光组化双标检测Nogo受体与RGC特异性标志物Brn3a的共存情况， Western blot检测视网膜Nogo受体表达，试剂盒检测视网膜丙二醛（MDA）含量，HE染色观察RGC数量。结果Brn3a与Nogo受体于视网膜内大量共存。与对照组相比，糖尿病组视网膜Nogo受体表达上调，MDA含量增加，RGC数量减少（均P＜0.001）；与糖尿病组相比，治疗组视网膜Nogo受体表达减少，MDA含量降低，RGC数量增加（P＜0.001）。结论 PTS可能通过抑制糖尿病大鼠视网膜RGC内Nogo受体的表达，抑制视网膜氧化应激，从而保护糖尿病视网膜RGC。
目的：探討三七三醇皂苷（PTS）對糖尿病大鼠視網膜神經節細胞（RGC）的保護作用及機製。方法SD大鼠隨機分為對照組、糖尿病組及治療組，糖尿病組及治療組腹腔註射鏈脲佐菌素誘導糖尿病動物模型，治療組給予PTS 50 mg·kg-1·d-1灌胃，1箇月後免疫熒光組化雙標檢測Nogo受體與RGC特異性標誌物Brn3a的共存情況， Western blot檢測視網膜Nogo受體錶達，試劑盒檢測視網膜丙二醛（MDA）含量，HE染色觀察RGC數量。結果Brn3a與Nogo受體于視網膜內大量共存。與對照組相比，糖尿病組視網膜Nogo受體錶達上調，MDA含量增加，RGC數量減少（均P＜0.001）；與糖尿病組相比，治療組視網膜Nogo受體錶達減少，MDA含量降低，RGC數量增加（P＜0.001）。結論 PTS可能通過抑製糖尿病大鼠視網膜RGC內Nogo受體的錶達，抑製視網膜氧化應激，從而保護糖尿病視網膜RGC。
목적：탐토삼칠삼순조감（PTS）대당뇨병대서시망막신경절세포（RGC）적보호작용급궤제。방법SD대서수궤분위대조조、당뇨병조급치료조，당뇨병조급치료조복강주사련뇨좌균소유도당뇨병동물모형，치료조급여PTS 50 mg·kg-1·d-1관위，1개월후면역형광조화쌍표검측Nogo수체여RGC특이성표지물Brn3a적공존정황， Western blot검측시망막Nogo수체표체，시제합검측시망막병이철（MDA）함량，HE염색관찰RGC수량。결과Brn3a여Nogo수체우시망막내대량공존。여대조조상비，당뇨병조시망막Nogo수체표체상조，MDA함량증가，RGC수량감소（균P＜0.001）；여당뇨병조상비，치료조시망막Nogo수체표체감소，MDA함량강저，RGC수량증가（P＜0.001）。결론 PTS가능통과억제당뇨병대서시망막RGC내Nogo수체적표체，억제시망막양화응격，종이보호당뇨병시망막RGC。
Objective To explore protective effects and potential underlying mechanisms of panax notoginseng (PTS) on retinal ganglion cell (RGC) in diabetic rats. Methods SD rats were randomly divided into control group, diabetic group and treatment group. The diabetic model rats were induced by intraperitoneal injection of streptozotocin. Rats were giv-en PTS 50 mg·kg-1·d-1 in treatment group. One month later, the coexistence of nogo receptor and Brn3a (special marker of RGC) was observed by immunofluorescence staining double-labeled method. The expression of Nogo receptor was detected by Western blot assay. The level of malondialdehyde (MDA) in retina was measured with detection kit. HE-staining was in-troduced to reveal the number of retinal RGC. Results A large number of Brn3a and Nogo receptors were co-existed in the retina. The Nogo receptor was exclusively expressed in RGC, which was up regulated in diabetic group compared with that of control group. The level of retinal MDA was increased and the number of RGC decreased in diabetic group than that of con-trol group (P<0.001). Compared with diabetic group, there were decreased retina Nogo receptor, decreased level of MDA and increased number of RGC in treatment group (P<0.001). Conclusion PTS attenuates diabetes-induced loss of RGC, which may ascribe for down-regulation of retina Nogo receptor and decreased oxidative stress.
