Renal Function in Analgesic Nephropathy

Comprehensive one-day renal function tests in 20 patients with a history of analgesic abuse showed varying degrees of chronic renal failure in all. There was no evidence of a selective defect in proximal tubular function, while a defective concentrating mechanism, usually considered necessary for the diagnosis of analgesic-induced renal damage, could be demonstrated in only 16 patients. A urinary acidification defect associated with a concentrating defect was found in nine cases and was thought to reflect specific collecting duct dysfunction. Urinary ammonium excretion was reduced in 13 subjects, owing to a reduced number of functioning nephrons or inadequate acidification, or both. Low citrate excretion was frequently encountered, and this, as well as defective urinary acidification, may play some part in predisposing patients with analgesic nephropathy to intrarenal calcification and progressive renal failure.     

绞股蓝多糖对糖尿病肾病大鼠肾功能的保护作用及其机制研究

目的:探讨绞股蓝多糖对糖尿病大鼠肾功能的影响及其保护的可能机制。方法:采用大鼠高脂高糖饲料结合腹腔注射链脲佐菌素建立2型糖尿病模型。灌胃给予绞股蓝多糖8周后,测定大鼠空腹血糖(FBG),血清肌酐、血清尿素氮、24 h尿量及尿蛋白等指标;组织病理切片观察肾形态,肾小球体积;Western blot法检测肾皮质NF-κB的表达。结果:绞股蓝多糖(GPS)可剂量依赖性的降低DN组的FBG、血肌酐、24 h尿量和尿蛋白;但血尿素氮模型组与GPS组无统计学差异;中、高剂量GPS治疗后,肾脏指数较模型组明显降低(P0.05);与模型组(149.8±12.2%)比较,高剂量GPS可抑制肾小球体积肥大至108.9±9.6%。进一步研究发现,GPS可剂量依赖性的降低DN组肾脏NF-κB蛋白的表达,高、中剂量组水平与模型组相比有统计学差异(P0.05)。结论:绞股蓝多糖对实验性糖尿病肾病具有保护作用,其机制可能与抑制肾炎症相关通路NF-κB的表达有关。     

西格列汀对早期2型糖尿病肾病患者肾功能的影响

目的:研究西格列汀对早期2型糖尿病肾病患者肾小球、肾小管标志性蛋白/酶的影响。方法:早期2型糖尿病肾病患者72例,随机数字表分为对照组36例、治疗组36例;两组均采用糖尿病饮食管理、运动治疗,在控制血糖、血脂、血压的基础上,治疗组给予磷酸西格列汀100 mg 1粒/次,1次/天,持续服药6月。观察治疗前、后两组血肌酐(Scr)、尿素氮(BUN)、糖化血红蛋白(Hb A1c)、血脂、空腹血糖(FBG)、餐后2小时血糖(2 h PBG)、血清胱抑素-C(Cys-C)及24 h尿微量白蛋白(24 h UAE)、尿N-乙酰-β-氨基葡萄糖苷酶(NAG)、尿β2-微球蛋白(β2-MG)的变化。结果:治疗后,治疗组血脂、Hb A1c、FBG、2 h PBG较对照组明显下降,差异有显著性(P0.05)。两组患者24 h UAE、NAG、β2-MG和Cys-C较治疗前均下降,差异有显著性(P0.05);两组治疗后相比,差异具有统计学意义(P0.05)。结论:西格列汀可以有效控制早期DN患者的血糖水平,减少血清Cys-C、尿微量白蛋白水平,减轻肾小管损伤,有利于延缓DN的病程和进展。     

卡托普利与坎地沙坦对老年糖尿病肾病患者肾功能的影响

目的:研究卡托普利联合坎地沙坦对糖尿病肾病患者肾功能的影响及临床疗效。方法:选择2014年5月-2015年5月我院收治的糖尿病肾病患者90例,根据治疗方法不同分为观察组和对照组。对照组给予卡托普利治疗,观察组在对照组基础上加用坎地沙坦治疗。观察并比较两组患者的临床疗效以及治疗前后空腹血糖、血尿素氮、血肌酐、24 h尿蛋白等水平的变化情况。结果:观察组的治疗总有效率为93.3%,对照组的治疗总有效率为84.4%;观察组患者的临床疗效显著高于对照组,但差异并不具有统计学意义(P0.05)。与治疗前比较,两组患者治疗后的空腹血糖、血尿素氮、血肌酐及24 h尿蛋白水平均显著降低,差异具有统计学意义(P0.05);治疗后,观察组患者的空腹血糖、血尿素氮、血肌酐和24 h尿蛋白值均显著均明显低于对照组,差异均具有统计学意义(P0.05)。结论:卡托普利联合坎地沙坦治疗糖尿病肾病较单独采用卡托普利治疗能够更加有效的改善患者的临床症状,保护患者的肾功能,具有较好的临床疗效。     

Ribose Supplementation Alone or with Elevated Creatine Does Not Preserve High Energy Nucleotides or Cardiac Function in the Failing Mouse Heart

Background

Reduced levels of creatine and total adenine nucleotides (sum of ATP, ADP and AMP) are hallmarks of chronic heart failure and restoring these pools is predicted to be beneficial by maintaining the diseased heart in a more favourable energy state. Ribose supplementation is thought to support both salvage and re-synthesis of adenine nucleotides by bypassing the rate-limiting step. We therefore tested whether ribose would be beneficial in chronic heart failure in control mice and in mice with elevated myocardial creatine due to overexpression of the creatine transporter (CrT-OE).

Methods and Results

Four groups were studied: sham; myocardial infarction (MI); MI+ribose; MI+CrT-OE+ribose. In a pilot study, ribose given in drinking water was bioavailable, resulting in a two-fold increase in myocardial ribose-5-phosphate levels. However, 8 weeks post-surgery, total adenine nucleotide (TAN) pool was decreased to a similar amount (8–14%) in all infarcted groups irrespective of the treatment received. All infarcted groups also presented with a similar and substantial degree of left ventricular (LV) dysfunction (3-fold reduction in ejection fraction) and LV hypertrophy (32–47% increased mass). Ejection fraction closely correlated with infarct size independently of treatment (r² = 0.63, p<0.0001), but did not correlate with myocardial creatine or TAN levels.

Conclusion

Elevating myocardial ribose and creatine levels failed to maintain TAN pool or improve post-infarction LV remodeling and function. This suggests that ribose is not rate-limiting for purine nucleotide biosynthesis in the chronically failing mouse heart and that alternative strategies to preserve TAN pool should be investigated.     

红花黄色素联合贝那普利对早期糖尿病肾病患者肾功能的影响

目的:探讨红花黄色素联合贝那普利对早期糖尿病肾病患者肾功能的影响。方法:选择2014年1月至2014年8月我院收治的120例早期糖尿病肾病患者为研究对象,并根据随机数字法,将其分为对照组(贝那普利治疗)和观察组(红花黄色素联合贝那普利治疗),每组各60例患者,观察和比较治疗前后两组患者中医证候变化情况、临床疗效以及血清胱抑素C(Cys C)、同型半胱氨酸(Hcy)、血肌酐(Scr)、尿素氮(BUN)、空腹血糖(FBG)、餐后2h血糖(2h PG)、糖化血红蛋白(Hb A1C)水平的变化情况。结果:与治疗前相比,两组治疗后的中医症候总积分、FBG、2h PG、Hb A1C、Cys C、Hcy、Scr、BUN水平均明显降低(P0.05);且观察组治疗后的中医症候总积分、FBG、2h PG、Hb A1C、Cys C、Hcy、Scr、BUN水平均明显低于对照组(P0.05)。观察组治疗的总有效率明显高于对照组(P0.05)。结论:红花黄色素联合贝那普利治疗能够较好地改善早期糖尿病肾病患者的肾功能,值得临床推广。     

西格列汀通过增加肾组织中SOCS 1和Podocalyxin的表达改善糖尿病肾病大鼠肾功能

目的:探讨西格列汀对糖尿病肾病大鼠肾功能及肾组织中细胞因子信号传导负调控因子1(Suppressors of cytockine signaling,SOCS 1)和足细胞特异蛋白抗体(Podocalyxin)表达的影响。方法:将大鼠随机分为4组:对照组,模型组,西格列汀组和贝那普利组。模型组、西格列汀组和贝那普利组采用腹腔注射链脲佐菌素建立模型,对照组给予腹腔注射等量生理盐水。造模成功后,西格列汀组(n=8)和贝那普利组(n=8)分别灌胃给予7 mg/kg/d的西格列汀和贝那普利。模型组(n=8)和对照组(n=10)均给予等体积的蒸馏水灌胃,连续8周。检测并对比各组大鼠代谢相关指标,肾组织纤维化程度指标,肾组织中炎症因子水平以及Podocalyxin、SOCS 1和结蛋白(Desmin)表达。结果:干预8周后,与对照组对比,模型组空腹血糖、糖化血红蛋白、甘油三酯、总胆固醇、24 h尿蛋白排泄率、肌酐、体重、肾组织转化生长因子-β1(Transforming growth factor,TGF-β1)、白介素(Interleukin,IL)-6、IL-1β、SOCS 1和Desmin水平均显著增加,Ⅳ型胶原蛋白(Collagen-Ⅳ,C-Ⅳ)、纤维连接蛋白(Fibronectin,FN)、层黏连蛋白(Laminin,LN)和Podocalyxin水平显著降低(P0.05);与模型组对比,西格列汀组和厄贝沙坦组空腹血糖、糖化血红蛋白、甘油三酯、总胆固醇、24 h尿蛋白排泄率、肌酐、体重、肾组织TGF-β1、IL-6、IL-1β和Desmin水平均显著降低,Podocalyxin和SOCS 1蛋白表达增加(P0.05)。但厄贝沙坦组与西格列汀组以上各指标对比差异无统计学意义(P0.05)。结论:西格列汀可能通过增加Podocalyxin和SOCS 1蛋白表达,降低肾组织中炎症因子和Desmin蛋白表达,进而改善糖尿病肾病大鼠肾纤维化和肾功能。     

Hydrogen Sulfide Alleviates Diabetic Nephropathy in a Streptozotocin-induced Diabetic Rat Model

Accumulating evidence has demonstrated that hydrogen sulfide (H₂S) plays critical roles in the pathogenesis of chronic kidney diseases. This study was designed to investigate whether H₂S has protective effects against diabetic nephropathy. Diabetic rats were induced by intraperitoneal injection of streptozotocin and administrated with H₂S donor NaHS for 12 weeks. Rat glomerular mesangial cells were pretreated with NaHS or MAPK inhibitors (U0126, SP600125, and SB203580) prior to high glucose exposure, and cell proliferation was determined. Our findings suggest that H₂S can improve renal function and attenuate glomerular basement membrane thickening, mesangial matrix deposition, and renal interstitial fibrosis in diabetic rats. H₂S was found to reduce high glucose-induced oxidative stress by activating the Nrf2 antioxidant pathway and to exert anti-inflammatory effects by inhibiting NF-κB signaling. In addition, H₂S reduced high glucose-induced mesangial cell proliferation by blockade of MAPK signaling pathways. Moreover, H₂S was also found to inhibit the renin-angiotensin system in diabetic kidney. In conclusion, our study demonstrates that H₂S alleviates the development of diabetic nephropathy by attenuating oxidative stress and inflammation, reducing mesangial cell proliferation, and inhibiting renin-angiotensin system activity.     

糖尿病肾病合并非糖尿病肾病的临床病理分析

目的：分析糖尿病肾病合并非糖尿病肾病的临床病理特点。方法：选取我院肾内科收治的临床诊断为糖尿病肾病的患者56 例,肾脏穿刺进行肾脏活体组织检查,通过病理诊断将患者分为两组,分别为糖尿病肾病组和糖尿病肾病合并非糖尿病肾病组, 比较两组患者的糖尿病病程、糖化血红蛋白、血压、血肌酐、血尿素氮、血尿酸、血清白蛋白、尿蛋白定量、血尿、视网膜病变。结果： 经肾脏组织活检,56例患者中NDRD 患者24 例(42.9%),DN患者32 例(57.1%);对24 例NDRD患者进行病理类型分类,其中IgA 肾病33.0%,膜性肾病25.0%、系膜增生性肾小球肾炎20.2%、高血压肾损害8.3%、微小病变4.2%、局灶节段硬化性肾炎4.2%、新 月体性肾小球肾炎4.2%。与DN组比较,NDRD 组糖尿病病程、糖化血红蛋白、血尿、视网膜病变均有差异(P＜0.05);而血肌酐、血 尿素氮、血尿酸、血清白蛋白、尿蛋白定量均无明显差异(P＞0.05)。结论：临床诊断的糖尿病肾病患者中有很大一部分实际上为糖 尿病肾病合并非糖尿病肾病,且以IgA 型肾病比较多见,糖尿病病程、糖化血红蛋白、血尿、视网膜病变对鉴别二者具有一定的指 导意义。     

Adipose-Derived Mesenchymal Stem Cells Transplantation Alleviates Renal Injury in Streptozotocin-Induced Diabetic Nephropathy

Previous studies have illustrated that bone marrow-derived mesenchymal stem cell (BMMSC) transplantation has therapeutic effects on diabetes and can prevent mice from renal damage and diabetic nephropathy (DN). Moreover, adipose-derived MSCs possess similar characteristics to BMMSCs. We investigated the effect of ADMSC transplantation on streptozotocin (STZ)-induced renal injury. Diabetes was induced in rats by STZ injection. After ADMSC treatment, renal histological changes and cell apoptosis were evaluated as were the expression of apoptosis-related proteins, Wnt/β-catenin pathway members, and klotho levels. We found that ADMSCs improved renal histological changes. Next, NRK-52E cells were exposed to normal glucose (NG; 5.5 mM glucose plus 24.5 mM mannitol)/high glucose (HG) or ADMSCs, and then measured for changes in the aforementioned proteins. Similarly, changes in these proteins were also determined following transient transfection of klotho siRNA. We found that both ADMSC transplantation and co-incubation reduced the rate of cellular apoptosis, decreased Bax and Wnt/β-catenin levels, and elevated Bcl-2 and klotho levels. Interestingly, klotho knockdown reversed the effects of ADMSCs on the expression of apoptosis-related proteins and Wnt/β-catenin pathway members. Taken together, ADMSCs transplantation might attenuate renal injury in DN via activating klotho and inhibiting the Wnt/β-catenin pathway. This study may provide evidence for the treatment of DN using ADMSCs.     

PDGF-BB Does Not Accelerate Healing in Diabetic Mice with Splinted Skin Wounds

Topical application of platelet-derived growth factor-BB (PDGF-BB) is considered to accelerate tissue repair of impaired chronic wounds. However, the vast literature is plagued with conflicting reports of its efficacy in animal models and this is often influenced by a wide array of experimental variables making it difficult to compare the results across the studies. To mitigate the confounding variables that influence the efficacy of topically applied PDGF-BB, we used a controlled full thickness splinted excisional wound model in db/db mice (type 2 diabetic mouse model) for our investigations. A carefully-defined silicone-splinted wound model, with reduced wound contraction, controlled splint and bandage maintenance, allowing for healing primarily by reepithelialization was employed. Two splinted 8 mm dorsal full thickness wounds were made in db/db mice. Wounds were topically treated once daily with either 3 µg PDGF-BB in 30 µl of 5% PEG-PBS vehicle or an equal volume of vehicle for 10 days. Body weights, wound contraction, wound closure, reepithelialization, collagen content, and wound bed inflammation were evaluated clinically and histopathologically. The bioactivity of PDGF-BB was confirmed by in vitro proliferation assay. PDGF-BB, although bioactive in vitro, failed to accelerate wound healing in vivo in the db/db mice using the splinted wound model. Considering that the predominant mechanism of wound healing in humans is by re-epeithelialization, the most appropriate model for evaluating therapeutics is one that uses splints to prevent excessive wound contraction. Here, we report that PDGF-BB does not promote wound closure by re-epithelialization in a murine splinted wound model. Our results highlight that the effects of cytoactive factors reported in vivo ought to be carefully interpreted with critical consideration of the wound model used.     

Establishment of an Inflamed Animal Model of Diabetic Nephropathy

Aims Inflammatory stress plays a crucial role in the progression of diabetic nephropathy (DN). This study aimed to establish a novel inflamed animal model of DN and to evaluate its significance in DN.Methods Nondiabetic db/m mice and diabetic db/db mice were randomly divided into four groups: db/m, db/m+casein, db/db, and db/db+casein for eight weeks. Casein was subcutaneously injected to induce chronic inflammation. Body weight and albumin to creatinine ratio (ACR) in the urine were measured every week. The plasma levels of serum amyloid protein A (SAA) and tumour necrotic factor-α (TNF-α) were determined with the enzyme-linked immunosorbent assay. The morphological changes to the renal pathology and ultra-microstructures were checked by pathological staining and electron microscopy. Immunofluorescent staining and Western blotting were used to determine the protein expression of podocyte-specific molecules and inflammatory cytokines in kidneys.Results ACR, plasma levels of SAA and TNF-α, protein expression of inflammatory cytokines, mesangial expansion, collagen accumulation, and foot process effacement in kidneys of casein-injected db/db mice were significantly increased compared with the db/db mice. Casein injection markedly decreased the protein expression of Wilms'' tumor-1 and nephrin in kidneys of db/db mice, which are specific podocyte biomarkers, suggesting that chronic inflammation accelerates podocyte injuries in db/db mice. Interestingly, no obvious urinary protein, inflammatory cytokine expression, or histological changes in the kidneys of casein-injected db/m mice were found compared with the db/m mice.Conclusion An inflamed animal model of DN was successfully established and may provide a useful tool for investigating the pathogenesis of DN under inflammatory stress.     

川芎嗪联合缬沙坦治疗糖尿病肾病肾衰竭的临床疗效观察

目的:探讨川芎嗪联合缬沙坦治疗糖尿病肾病肾衰竭的临床疗效。方法:选择我院2011年1月至2013年1月收治的糖尿病肾病肾衰竭患者96例,并将其随机分为实验组和对照组,每组48例。两组患者均根据病情给予对症支持治疗,并严格控制血糖。在常规治疗基础上,实验组患者给予川芎嗪注射液240 mg,静脉滴注,1次/d,同时给予缬沙坦80 mg,口服,1次/d,21天为1个疗程;对照组患者给予缬沙坦80 mg,口服,1次/d,21天为1个疗程。1个疗程后观察两组患者的临床疗效、血液学指标、尿检指标等实验室检查。结果:治疗21天后,实验组的临床有效率达83.3%,显著高于对照组(60.4%),差异具有统计学意义(P0.05);两组空腹血糖、尿蛋白、尿素氮、血肌酐水平均较治疗前显著改善,且实验组以上指标及胆固醇水平的改善程度明显优于对照组,差异有统计学意义(P0.05)。治疗过程中,两组均无严重不良反应发生。结论:川芎嗪联合缬沙坦可以更有效地改善糖尿病肾病肾衰竭患者的临床疗效,有一定的临床应用价值。     

C肽对糖尿病大鼠肾脏的影响

比较C肽和胰岛素对大鼠糖尿病肾病的治疗作用。方法:选取Wistar大鼠40只,分为正常对照组(NG组)和糖尿病组(DM组),糖尿病组链脲佐菌素诱发大鼠成模后,随机分为三组:糖尿病组(DM组)、胰岛素组(IG组)和C肽组(ICG组)。治疗8周后测定各组大鼠24小时尿白蛋白排泄率(UAER)、肾重/体重,并观察糖尿病大鼠肾脏超微结构变化。结果:24小时尿白蛋白排泄率:糖尿病组明显增加,C肽组明显低于糖尿病组和胰岛素组,差异具有显著性。大鼠肾脏超微结构变化:各组大鼠肾小球截面积、肾小球平均体积(MGV)、细胞外基质/肾小球截面积比值、细胞外基质截面积、肾小球基底膜厚度相比,糖尿病组明显升高,C肽组较胰岛素组和糖尿病组明显下降,差异具有显著性。结论:C肽治疗可以降低24小时尿白蛋白排泄率,改善糖尿病大鼠肾脏超微结构病变。     

丹蛭降糖胶囊联合胰激肽原酶治疗2型糖尿病早期肾病的疗效及对肾功能、血糖指标的影响

摘要 目的：研究丹蛭降糖胶囊联合胰激肽原酶治疗2型糖尿病早期肾病的疗效及对肾功能、血糖指标的影响。方法：选择2021年1月～2022年7月于我院诊治的60例2型糖尿病早期肾病患者,将其随机分为两组。对照组单用胰激肽原酶治疗,观察组采用丹蛭降糖胶囊联合胰激肽原酶治疗。检测两组的肾功能指标、血糖指标[空腹血糖（FPG）、胰岛素抵抗指数（HOMA-IR）、空腹C肽（FCP）、餐后2 h血糖（PBG）、糖化血红蛋白（HbAlc）和餐后2hC肽（PCP）],且检测两组的超敏C反应蛋白（hs-CRP）水平。结果：观察组的有效率高于对照组（P<0.05）;治疗后,两组的血清hs-CRP水平均降低,且观察组较对照组低（P<0.05）;治疗后,两组的血清肌酐、β2-微球蛋白、尿素和胱抑素C水平明显降低（P<0.05）,且观察组的血清肌酐、β2-微球蛋白、尿素和胱抑素C水平明显低于对照组（P<0.05）;治疗后,两组的FPG、HOMA-IR、FCP、PBG、HbAlc和PCP水平均明显降低（P<0.05）,且观察组的FPG、HOMA-IR、FCP、PBG、HbAlc和PCP水平明显低于对照组（P<0.05）。结论：丹蛭降糖胶囊联合胰激肽原酶对2型糖尿病早期肾病有显著的疗效,能明显改善肾功能和血糖指标。     

4-Aminopyridine Does Not Enhance Flocculus Function in Tottering,a Mouse Model of Vestibulocerebellar Dysfunction and Ataxia

The potassium channel antagonist 4-aminopyridine (4-AP) improves a variety of motor abnormalities associated with disorders of the cerebellum. The most rigorous quantitative data relate to 4-AP''s ability to improve eye movement deficits in humans referable to dysfunction of the cerebellar flocculus. Largely based on work in the ataxic mouse mutant tottering (which carries a mutation of the Cacna1a gene of the P/Q voltage-activated calcium channel), 4-AP is hypothesized to function by enhancing excitability or rhythmicity of floccular Purkinje cells. We tested this hypothesis by determining whether systemic or intrafloccular administration of 4-AP would ameliorate the eye movement deficits in tottering that are attributable to flocculus dysfunction, including the reductions in amplitude of the yaw-axis vestibulo-ocular reflex (VOR) and vision-enhanced vestibulo-ocular reflex (VVOR), and the optokinetic reflex (OKR) about yaw and roll axes. Because tottering''s deficits increase with age, both young and elderly mutants were tested to detect any age-dependent 4-AP effects. 4-AP failed to improve VOR, VVOR, and OKR gains during sinusoidal stimuli, although it may have reduced the tendency of the mutants'' responses to VOR and VVOR to decline over the course of a one-hour recording session. For constant-velocity optokinetic stimuli, 4-AP generated some enhancement of yaw OKR and upward-directed roll OKR, but the effects were also seen in normal C57BL/6 controls, and thus do not represent a specific reversal of the electrophysiological consequences of the tottering mutation. Data support a possible extra-floccular locus for the effects of 4-AP on habituation and roll OKR. Unilateral intrafloccular 4-AP injections did not affect ocular motility, except to generate mild eye elevations, consistent with reduced floccular output. Because 4-AP did not produce the effects expected if it normalized outputs of floccular Purkinje cells, there is a need for further studies to elucidate the drug''s mechanism of action on cerebellar motor dysfunction.     

Probiotic Soy Milk Consumption and Renal Function Among Type 2 Diabetic Patients with Nephropathy: a Randomized Controlled Clinical Trial

Probiotics and Antimicrobial Proteins - Diabetic nephropathy (DN) is one the most important complications of diabetes leading to end-stage renal disease. Dietary approaches have been considered to...     

金樱子提取液对糖尿病肾病大鼠的肾脏保护作用

目的:研究金樱子提取液对糖尿病肾病(Diabetic Nephropathy,DN)大鼠的肾脏保护作用。方法:在高糖高脂饲料喂食SD(Sprague-Dawley)大白鼠的基础上腹腔注射链脲佐菌素(streptozotocin,STZ)诱导糖尿病肾病大鼠模型,随机分为糖尿病肾病模型组(DN组)和金樱子治疗组(DN+RLM组),同时另设正常对照组(NC组)和金樱子对照组(NC+RLM组)。检测金樱子提取液对各组大鼠血糖(fasting blood-glucose,FBG)、糖化血红蛋白(glycosylated haemoglobin,GHb)、24小时尿微量白蛋白和尿量、血尿素氮(BUN)、血肌酐(Scr)、胆固醇(TC)、甘油三酯(TG)及肾脏结构的影响。结果:与DN大鼠相比,糖尿病肾病大鼠经金樱子提取液治疗后,大鼠FBG、GHb水平、24 h尿微量白蛋白、24 h尿量、肾脏指数明显降低,血脂紊乱、肾功能损害以及DN肾脏病理明显改善,且无明显副作用。结论:金樱子提取液可明显降低DN大鼠血糖,改善DN大鼠血脂、肾功能紊乱及肾脏病理变化,对糖尿病大鼠肾脏具有较强的保护作用。     

Sunitinib Does Not Accelerate Tumor Growth in Patients with Metastatic Renal Cell Carcinoma

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Highlights? Drugs targeting the tumor vasculature are under investigation for cancer treatment ? However, changes in tumor vasculature may promote tumor growth and/or tumor spread ? Our analysis shows that sunitinib does not accelerate tumor growth in humans ? Sunitinib administration has positive effects and no negative effects when stopped