CAJ | 학술논문

目的：探讨养阴活血方药对糖尿病大鼠肾脏线粒体氧化应激损伤的影响及相关机制。方法将SD大鼠分为三组，正常对照组(NC组)、糖尿病对照组(DM组)和养阴活血方药治疗组(NYPBR组)，后两组应用链脲佐菌素(STZ)制造糖尿病大鼠模型。NYPBR组大鼠给予养阴活血方药防治。10周末，测定各组大鼠血糖、体重、肾重、血肌酐(SCr)、24 h尿蛋白，检测肾脏线粒体丙二醛(MDA)含量及谷胱甘肽过氧化物酶(GSH-Px)、一氧化氮合酶(NOS)、Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶和琥珀酸脱氢酶(SDH)的活性，透射电镜观察肾组织超微结构变化。结果与NC组比较，DM组大鼠肾脏线粒体MDA[(1.34±0.24)nmol/mg]、GSH-Px[(57.63±4.91)U/mg]及NOS [(0.81±0.07)U/mg]明显升高(均 P <0.01)，Na+-K+-ATP酶[(1.40±0.10)μmol/(mg·h)]、Ca2+-Mg2+-ATP酶[(1.43±0.10)μmol/(mg·h)]和SDH[(24.33±2.31)U/mg]显著降低(均P<0.01)，肾功能减退，肾脏组织发生病理性改变，线粒体出现损伤。养阴活血方药可显著改善上述变化，NYPBR组的MDA[(0.81±0.08)nmol/mg]、GSH-Px[(50.55±5.86)U/mg]及NOS[(0.72±0.07)U/mg]均低于DM组(P<0.01或P<0.05)，Na+-K+-ATP酶[(1.66±0.18)μmol/(mg·h)]、Ca2+-Mg2+-ATP酶[(1.76±0.20)μmol/(mg·h)]和SDH[(40.92±3.77)U/mg]明显上升(P<0.05或P<0.01)。结论糖尿病大鼠肾脏线粒体存在明显的氧化应激损伤，NYPBR可显著减轻糖尿病大鼠肾脏线粒体损伤，此作用可能与降低NOS活性，提高SDH、Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性有关。
목적：탐토양음활혈방약대당뇨병대서신장선립체양화응격손상적영향급상관궤제。방법장SD대서분위삼조，정상대조조(NC조)、당뇨병대조조(DM조)화양음활혈방약치료조(NYPBR조)，후량조응용련뇨좌균소(STZ)제조당뇨병대서모형。NYPBR조대서급여양음활혈방약방치。10주말，측정각조대서혈당、체중、신중、혈기항(SCr)、24 h뇨단백，검측신장선립체병이철(MDA)함량급곡광감태과양화물매(GSH-Px)、일양화담합매(NOS)、Na+-K+-ATP매、Ca2+-Mg2+-ATP매화호박산탈경매(SDH)적활성，투사전경관찰신조직초미결구변화。결과여NC조비교，DM조대서신장선립체MDA[(1.34±0.24)nmol/mg]、GSH-Px[(57.63±4.91)U/mg]급NOS [(0.81±0.07)U/mg]명현승고(균 P <0.01)，Na+-K+-ATP매[(1.40±0.10)μmol/(mg·h)]、Ca2+-Mg2+-ATP매[(1.43±0.10)μmol/(mg·h)]화SDH[(24.33±2.31)U/mg]현저강저(균P<0.01)，신공능감퇴，신장조직발생병이성개변，선립체출현손상。양음활혈방약가현저개선상술변화，NYPBR조적MDA[(0.81±0.08)nmol/mg]、GSH-Px[(50.55±5.86)U/mg]급NOS[(0.72±0.07)U/mg]균저우DM조(P<0.01혹P<0.05)，Na+-K+-ATP매[(1.66±0.18)μmol/(mg·h)]、Ca2+-Mg2+-ATP매[(1.76±0.20)μmol/(mg·h)]화SDH[(40.92±3.77)U/mg]명현상승(P<0.05혹P<0.01)。결론당뇨병대서신장선립체존재명현적양화응격손상，NYPBR가현저감경당뇨병대서신장선립체손상，차작용가능여강저NOS활성，제고SDH、Na+-K+-ATP매화Ca2+-Mg2+-ATP매활성유관。
Objective To investigate the effect of Nourishing Yin and Promoting Bloodflow Recipe (NYPBR) on the ox-idative stress injuries in renal mitochondria of diabetic rats and related mechanism. Methods SD rats were divided into 3 groups:normal control group (NC group), diabetes control group (DM group) and NYPBR group, the latter 2 groups diabetes rat models were created by streptozotocin (STZ). The NYPBR group was treated with NYPBR. At the end of 10 weeks, blood sugar, body weight, kidney weight, serum creatinine (SCr), 24-hour urine protein were measured, and con-tent or activity of renal mitochondria MDA and glutathion peroxidase (GSH-Px), nitric oxide synthase (NOS), ATPase and succinate dehydrogenase (SDH) were determined for each of the 3 groups, and ultrastructure of renal tissue was observed with transmission electron microscope. Results Compared with NC group, renal mitochondria MDA [(1.34±0.24) nmol/mg], GSH-Px [(57.63±4.91) U/mg] and NOS [(0.81±0.07) U/mg] of DM group were elevated significantly (all P< 0.01), the activities of Na+-K+-ATPase [(1.40±0.10) μmol/(mg·h)], Ca2+-Mg2+-ATPase [(1.43±0.10)μmol/(mg·h)] and SDH [(24.33±2.31) U/mg] decreased greatly (all P< 0.01), and there were renal pathological changes and mito-chondria injury. NYPBR could improve the changes. Compared with DM group, renal mitochondria MDA [(0.81±0.08) nmol/mg], GSH-Px (50.55±5.86) U/mg] and NOS [(0.72±0.07) U/mg] of NYPBR group were decreased significantly (P< 0.01 or P<0.05),Na+-K+-ATPase [(1.66±0.18) μmol/(mg·h)], Ca2+-Mg2+-ATPase [(1.76±0.20)μmol/(mg·h)] and SDH [(40.92±3.77) U/mg] elevated greatly (P<0.05 or P<0.01). Conclusion Oxidative stress injuries occur in diabetes rat mitochondria. NYPBR may significantly decrease the injuries of diabetes rat renal mitochondria, which may be related to decreasing in NOS activity, and increasing in SDH, Na+-K+-ATPase and Ca2+-Mg2+-ATPase.