医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2015年
5期
593-597
,共5页
聂寒%苏珂%龙艳%蒋姗姗
聶寒%囌珂%龍豔%蔣姍姍
섭한%소가%룡염%장산산
青蒿琥酯%肾病,糖尿病%肿瘤坏死因子%单核细胞趋化蛋白
青蒿琥酯%腎病,糖尿病%腫瘤壞死因子%單覈細胞趨化蛋白
청호호지%신병,당뇨병%종류배사인자%단핵세포추화단백
Artesunate%Nephropathy,diabetic%Tumor necrosis factor-α%Monocyte chemotactic protein-1
目的:观察青蒿琥酯对糖尿病肾病大鼠肾功能及单核细胞趋化蛋白-1(MCP-1)、肿瘤坏死因子-α(TNF-α)表达的影响。方法雄性斯泼累格·多雷( SD)大鼠36只,随机分为6组,每组6只:正常对照组,模型对照组,青蒿琥酯小剂量组(10 mg·kg-1·d-1)、中剂量组(20 mg·kg-1·d-1)、大剂量组(30 mg·kg-1·d-1),依那普利组(10 mg·kg-1·d-1)。采用高糖高脂饮食联合一次性腹腔注射小剂量链脲佐菌素法建立2型糖尿病肾病模型。分别干预8周后,检测各组大鼠血糖、24 h尿蛋白定量、血肌酐、尿素氮等评估肾功能情况;光镜下观察肾组织病理形态学变化;检测大鼠血清MCP-1、TNF-α水平。结果与模型对照组比较,各治疗组24 h尿蛋白、血肌酐、血尿素氮、血糖均一定程度下降(均P<0.01),尤以青蒿琥酯中、大剂量组下降更显著(均P<0.01)。模型对照组MCP-1及TNF-α的含量分别为(181.71±23.06),(3.98±0.24) pg·mL-1;青蒿琥酯小剂量组分别为(157.47±38.53),(3.14±0.38) pg·mL-1,中剂量组分别为(138.65±18.03),(2.58±0.11) pg·mL-1,大剂量组分别为(105.09±12.64),(2.25±0.16) pg·mL-1,均显著降低(均P<0.05)。结论青蒿琥酯对2型糖尿病肾病具有一定的治疗作用,其机制可能部分是通过减少炎性因子MCP-1、TNF-α的分泌,抑制肾脏炎性反应,调节肾功能,缓解肾脏的病理损伤,从而延缓肾脏病变的发展。
目的:觀察青蒿琥酯對糖尿病腎病大鼠腎功能及單覈細胞趨化蛋白-1(MCP-1)、腫瘤壞死因子-α(TNF-α)錶達的影響。方法雄性斯潑纍格·多雷( SD)大鼠36隻,隨機分為6組,每組6隻:正常對照組,模型對照組,青蒿琥酯小劑量組(10 mg·kg-1·d-1)、中劑量組(20 mg·kg-1·d-1)、大劑量組(30 mg·kg-1·d-1),依那普利組(10 mg·kg-1·d-1)。採用高糖高脂飲食聯閤一次性腹腔註射小劑量鏈脲佐菌素法建立2型糖尿病腎病模型。分彆榦預8週後,檢測各組大鼠血糖、24 h尿蛋白定量、血肌酐、尿素氮等評估腎功能情況;光鏡下觀察腎組織病理形態學變化;檢測大鼠血清MCP-1、TNF-α水平。結果與模型對照組比較,各治療組24 h尿蛋白、血肌酐、血尿素氮、血糖均一定程度下降(均P<0.01),尤以青蒿琥酯中、大劑量組下降更顯著(均P<0.01)。模型對照組MCP-1及TNF-α的含量分彆為(181.71±23.06),(3.98±0.24) pg·mL-1;青蒿琥酯小劑量組分彆為(157.47±38.53),(3.14±0.38) pg·mL-1,中劑量組分彆為(138.65±18.03),(2.58±0.11) pg·mL-1,大劑量組分彆為(105.09±12.64),(2.25±0.16) pg·mL-1,均顯著降低(均P<0.05)。結論青蒿琥酯對2型糖尿病腎病具有一定的治療作用,其機製可能部分是通過減少炎性因子MCP-1、TNF-α的分泌,抑製腎髒炎性反應,調節腎功能,緩解腎髒的病理損傷,從而延緩腎髒病變的髮展。
목적:관찰청호호지대당뇨병신병대서신공능급단핵세포추화단백-1(MCP-1)、종류배사인자-α(TNF-α)표체적영향。방법웅성사발루격·다뢰( SD)대서36지,수궤분위6조,매조6지:정상대조조,모형대조조,청호호지소제량조(10 mg·kg-1·d-1)、중제량조(20 mg·kg-1·d-1)、대제량조(30 mg·kg-1·d-1),의나보리조(10 mg·kg-1·d-1)。채용고당고지음식연합일차성복강주사소제량련뇨좌균소법건립2형당뇨병신병모형。분별간예8주후,검측각조대서혈당、24 h뇨단백정량、혈기항、뇨소담등평고신공능정황;광경하관찰신조직병리형태학변화;검측대서혈청MCP-1、TNF-α수평。결과여모형대조조비교,각치료조24 h뇨단백、혈기항、혈뇨소담、혈당균일정정도하강(균P<0.01),우이청호호지중、대제량조하강경현저(균P<0.01)。모형대조조MCP-1급TNF-α적함량분별위(181.71±23.06),(3.98±0.24) pg·mL-1;청호호지소제량조분별위(157.47±38.53),(3.14±0.38) pg·mL-1,중제량조분별위(138.65±18.03),(2.58±0.11) pg·mL-1,대제량조분별위(105.09±12.64),(2.25±0.16) pg·mL-1,균현저강저(균P<0.05)。결론청호호지대2형당뇨병신병구유일정적치료작용,기궤제가능부분시통과감소염성인자MCP-1、TNF-α적분비,억제신장염성반응,조절신공능,완해신장적병리손상,종이연완신장병변적발전。
Objective To investigate the effects of artesunate( Art) on renal function and the expression of monocyte chemotactic protein-1(MCP-1)and tumor necrosis factor-α(TNF-α)in rats with type 2 diabetic nephropathy(DN). Methods Thirty six male SD rats were randomly divided into six groups, six rats in each, as the normal control, model control, low-dose Art, middle-dose Art, high-dose Art groups which were intragastrically administrated with Art at the dose of 10, 20 and 30 mg·kg-1 ·d-1 for consecutive 8 weeks, enalapril group, which were intragastrically administrated with enalapril 10 mg·kg-1 ·d-1 for consecutive 8 weeks. Rats were injected with low dosage streptozotocin and fed with high fat and high sugar diets to establish type 2 diabetic nephropathy rat model. After 8 weeks’ treatment, the plasma glucose, 24-hour urine protein, serum creatinine and blood urea nitrogen were measured to evaluate renal function. The pathological morphology of rats was performed. Immunohistochemistry and enzyme linked immunosorbent assay ( ELISA ) were performed to examine the expression levels of MCP-1 and TNF-α,respectively. Results Compared with the model control group, 24-hour urine protein, serum creatinine, blood urea nitrogen and blood glucose were significantly decreased in the treatment groups (P<0. 01). Art significantly decreased the serum expressions of MCP-1 and TNF-α in low-, middle-, high-dose Art group ( 157. 47 ± 38. 53, 138.65±18.03,105.09±12. 64 and 3. 14±0. 38,2. 58±0. 11,2. 25±0. 16) pg·mL-1, compared with model control group (181.71±23.06 and 3. 98±0. 24) pg·mL-1(P<0. 05). Conclusion Art has beneficial effects on type 2 diabetic nephropathy. The mechanism of which may be related to the inhibition of inflammatory factor MCP-1 and TNF-α,further relive the pathological injury of kidney and delay the progress of diabetic nephropathy to some extent.