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1.
ＩＮＴＲＯＤＵＣＴＩＯＮＣｉｓ ｄｉａｍｍｉｎｅｄｉｃｈｌｏｒｏｐｌａｔｉｎｕｍ (Ⅱ ) (Ｃｉｓ ｐｌａｔｉｎ)ｉｓａｗｉｄｅｌｙｕｓｅｄａｎｔｉｎｅｏｐｌａｓｔｉｃａｇｅｎｔｔｈａｔｈａｓｎｅｐｈｒｏｔｏｘｉｃｉｔｙａｓａｍａｊｏｒｄｏｓｅ ｌｉｍｉｔｉｎｇｓｉｄｅｅｆｆｅｃｔ.Ｔｈｅｍｏｓｔｃｏｍｍｏｎｆｏｒｍｏｆｃｉｓｐｌａｔｉｎ ｉｎ ｄｕｃｅｄｒｅｎａｌｔｏｘｉｃｉｔｙｉｓｎｏｎ ｏｌｉｇｕｒｉｃａｃｕｔｅｒｅｎａｌｆａｉｌｕｒｅ.Ｔｈｅｕｎｄｅｒｌｙｉｎｇｍｅｃｈａｎｉｓｍｏｆｔｈｉｓｒｅｎａ…  相似文献   

2.
This study was carried out to elucidate the nephroprotective effects from a mixture of 8 L-amino acids and the possible mechanism of protection by this amino acid mixture. Acute renal failure model was induced by an intravenous administration of 10 mg/kg cisplatin to male Sprague-Dawley rats. A mixture of 8 L-amino acids or 0.9% saline was infused at a rate of 2 ml/h for 3 h, starting with a 2 ml bolus injection before cisplatin administration. Amino acids showed no acute effect on renal morphology. The infusion of a mixture of 8 L-amino acids increased GFR by 85% in control rats. The abnormalities of urine sodium and potassium excretion caused by cisplatin were markedly attenuated by the administration of the amino acid mixture. With the infusion of this amino acid mixture, cisplatin-induced abnormal state 4 respiration returned to control levels and the depressed state 3 respiration, respiratory control ratio and carbonyl cyanide p-trifluoromethoxyphenyl hydrazone-uncoupled respiration were ameliorated remarkably. A mixture of 8 L-amino acids showed marked nephroprotection against cisplatin-induced acute renal failure in rats and might function through augmentation of the cisplatin-injured renal mitochondrial electron transport-oxidative phosphorylation sequence, probably via stabilizing the membrane (including inner mitochondrial membrane) protein tertiary structure. In addition, this amino acid mixture remarkably increased GFR and decreased urine sodium excretion in rats.  相似文献   

3.
ＩＮＴＲＯＤＵＣＴＩＯＮＡｃｕｔｅｒｅｎａｌｆａｉｌｕｒｅ(ＡＲＦ),ｕｓｕａｌｌｙｒｅｆｅｒｒｅｄｔｏａｓａｃｕｔｅｔｕｂｕｌａｒｎｅｃｒｏｓｉｓ,ｉｓａｃｏｍｍｏｎｓｙｎｄｒｏｍｅｃｈａｒａｃｔｅｒｉｚｅｄｂｙａｎａｂｒｕｐｔａｎｄｓｕｓｔａｉｎｅｄｄｅｃｌｉｎｅｉｎｇｌｏｍｅｒｕｌａｒｆｉｌｔｒａｔｉｏｎｗｉｔｈｒｅｓｕｌｔａｎｔａｚｏｔｅｍｉａ,ｃａｕｓｅｄｂｙａｃｕｔｅｉｓｃｈｅｍｉｃａｎｄ/ｏｒｔｏｘｉｃｉｎｊｕｒｉｅｓ.Ｉｔｉｓｎｏｔｉｍｍｅｄｉａｔｅｌｙｒｅｖｅｒｓｉｂｌｅｗｈｅｎｃａ…  相似文献   

4.

Background and objective

It has been shown that macrophages play an important role in the development of severe acute pancreatitis (SAP), and eventually lead to multiple organ failure (MOF). Clodronate-liposome selectively depleted macrophages. This study was to investigate the role of renal macrophage infiltration in acute renal injury in rats with SAP and to evaluate the potential of superparamagnetic iron oxide (SPIO)-enhanced magnetic resonance imaging (MRI) for diagnosis.

Methods

Superparamagnetic Fe3O4 nanoparticles were prepared by chemical coprecipitation. SPIO-liposomes and SPIO-clodronate-liposomes were prepared by the thin film method. SAP models were prepared by injection of sodium taurocholate into the subcapsular space of rat pancreas. Sprague-Dawley rats were randomly divided into a control group, SAP plus SPIO-liposome (P) group, and SAP plus SPIO-clodronate-containing liposome (T) group. Kidney injury was evaluated by T2-weighted MRI scan. The levels of serum amylase (SAM), blood urea nitrogen (BUN), and serum creatinine (SCr) were measured by an automated enzymatic method. Serum tumor necrosis factor-α (TNF-α) was measured by enzyme-linked immunosorbent assay (ELISA). Pathological changes in the pancreas and kidney were observed using hematoxylin and eosin (H&E) staining, while cell apoptosis was detected with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. In addition, the macrophage markers (CD68) of the renal tissue were detected with immunohistochemistry.

Results

The pathological changes in the pancreas and kidneys of rats in the T group were milder than those in the P group. The MRI signal intensity of the kidneys in the P and T groups was significantly lower than that in the control group. There were significant changes in the two experimental groups (P<0.01). The levels of SAM, Bun, SCr, and TNF-α in rats in the P group were higher than those in the control group (P<0.01) and in the T group (P<0.01). The apoptosis of the kidney in the T group was higher than that in the P group at 2 and 6 h (P<0.01).

Conclusions

Clodronate-containing liposomes protected against renal injury in SAP rats, and SPIO can be used as a tracer for MRI examination to detect renal injury in SAP rats. SPIO-aided MRI provided an efficient non-invasive way to monitor the migration of macrophages after renal injury in rats with SAP.  相似文献   

5.
目的:探讨两种家兔急性肾功能衰竭(ARF)模型的方法学差异.方法:皮下注射1%HgCl2(1.5ml/kg.bw,H组)、肌肉注射50%甘油(5.6ml/kg.bw、8ml/kg.bw、10ml/kg.bw三种剂量,依次为G1组、G2组、G3组)复制家兔ARF模型,测定24h和48h血清尿素氮(BUN)和肌酐(Cre)水平,观察比较各组模型复制的成功率、存活率及稳定性.结果:G1、G2两组不能成功复制ARF模型;G3组BUN、Cre较H组降低(P＜0.05).但G3组的存活率及稳定性均显著高于H组(P＜0.05).结论:两种模型复制方法各有优缺点,应根据不同研究目的选择相应的模型.  相似文献   

6.
冰片在中风及假手术大鼠体内的药代动力学研究(英文)简   总被引：1，自引：0，他引：1  
Objective： This study was designed to investigate the pharmacokinetics of borneol in the pathological conditions of stroke and evaluate the pharmacokinetic differences of borneol caused by stroke after oral administration of borneol and Xingnaojing （XNJ）. Methods： The rats were divided into two groups, ischemia-reperfusion （IR） and sham-operated （SO） rats. Each group contained two subgroups： pure borneol and XNJ subgroups. After administration with the same dosages of borneol 162.0 mg/kg, plasma samples were collected. The cerebral ischemia-reperfusion model was created by reversible middle cerebral artery occlusion （MCAO）. The blood samples were collected punc- tually after oral administration and a specific gas chromatographic system-flame ionization detector （GC-FID） method was developed and employed to determine the level of borneol in the plasma. The pharmacokinetic parameters were analyzed using non-compartmental methods with Kinetica. Results： After administration of borneol, the maximum plasma concentration （Cmax） and area under the curve （AUC） values in stroke rats significantly increased by 302% and 275%, respectively, compared with the SO rats, and the same phenomenon appeared after administration of XNJ. In the rats with the same physiological conditions, the Cmax and AUC had higher values in the borneol subgroup （P〈0.05）. Conclusions： These results suggest that the pathological damages of ischemia-reperfusion have a significant impact on the pharmacokinetic traits of borneol and that there are some components in XNJ inhibiting the absorption of borneol.  相似文献   

7.
Background and objective: Gonadotropin-releasing hormone (GnRH) plays an important role in the regulation of ovarian function and ovarian cancer cell growth. In this study, we determined whether administration of the GnRH agonist (GnRHa), triporelin, prior to cisplatin treatment affects cisplatin and/or prevents cisplatin-induced ovarian damage. Methods: nu/nu mice were injected with ovarian cancer OVCAR-3 cells intraperitoneally. After two weeks, the mice were treated with saline (control), cisplatin, GnRHa, or cisplatin plus GnRHa for four weeks. At the end of the experimental protocol, blood, tumor, ovary, and uterine tissues were resected for hematoxylin and eosin (H&E) staining, immunohistochemical analyses of Ki67, nuclear factor-κB (NF-κB), and caspase-3, transmission electron microscopy of apoptosis, or enzyme-linked immunosorbent assay (ELISA) analyses of anti-Mullerian hormone (AMH). Results: Cisplatin treatment effectively inhibited tumor growth in mice treated with human ovarian cancer cells; however the treatment also induced considerable toxicity. Immunohistochemical analyses showed that Ki67 expression was reduced in cisplatin-treated mice compared to control (P<0.05), but there was no statistically significant differences between cisplatin-treated mice and cisplatin plus GnRHa-treated mice (P>0.05), while expressions of NF-κB and caspase-3 were reduced and induced, respectively, in cisplatin-treated mice and cisplatin plus GnRHa-treated mice. Apoptosis occurred in the GnRHa, cisplatin, and cisplatin plus GnRHa-treated mice, but not in control mice. Ovaries exposed to GnRHa in both GnRHa mice and cisplatin-treated mice (combination group) had significantly more primordial and growth follicles and serum levels of AMH than those in the control mice and cisplatin-treated mice (P<0.05). Conclusions: Administration of GnRHa to mice significantly decreased the extent of ovarian damage induced by cisplatin, but did not affect the anti-tumor activity of cisplatin.  相似文献   

8.

Objective

The present study aims at determining the stability of a popular type 2 diabetes rat model induced by a high-fat diet combined with a low-dose streptozotocin injection.

Methods

Wistar rats were fed with a high-fat diet for 8 weeks followed by a one-time injection of 25 or 35 mg/kg streptozotocin to induce type 2 diabetes. Then the diabetic rats were fed with regular diet/high-fat diet for 4 weeks. Changes in biochemical parameters were monitored during the 4 weeks.

Results

All the rats developed more severe dyslipidemia and hepatic dysfunction after streptozotocin injection. The features of 35 mg/kg streptozotocin rats more resembled type 1 diabetes with decreased body weight and blood insulin. Rats with 25 mg/kg streptozotocin followed by normal diet feeding showed normalized blood glucose level and pancreatic structure, indicating that normal diet might help recovery from certain symptoms of type 2 diabetes. In comparison, diabetic rats fed with high-fat diet presented decreased but relatively stable blood glucose level, and this was significantly higher than that of the control group (P&gt;0.05).

Conclusions

This model easily recovers with normal diet feeding. A high-fat diet is suggested as the background diet in future pharmacological studies using this model.
  相似文献   

9.
目的：观察戊四氮（PTZ）致痫大鼠海马神经元caspase-3表达以及中药复方AAP的脑保护作用.方法：144只健康成年雄性Wistar大鼠随机分为对照组（CK组）、模型组（PTZ组）、中药大剂量组（AAPl组）、中药中剂量组（AAPm组）、中药小剂量组（AAPs组）和丙戊酸钠组（VPA组）;每组各6只.CK组和PTZ组分别给予生理盐水（4mL/kg.d）灌胃;中药各组分别给予中药复方大、中、小剂量（10.26g/kg、5.13g/kg、2.56g/kg）灌胃,每天1次;VPA组腹腔注射VPA（20mg/kg.d）.造模第一天,除CK组外,其余各组大鼠均腹腔注射戊四氮（PTZ）75mg/kg,观察记录大鼠行为学变化;于致痫后12h、2d、5d、7d相应时间点取材,制备脑标本;免疫组化检测caspase-3表达.结果：致痫后,除CK组外,其余各组海马区caspase-3阳性表达增强;7天,与PTZ组相比,AAPl组、AAPm组和AAPs组海马CA3区caspase-3阳性表达减弱（P〈0.05）.结论：caspase-3参与致痫大鼠海马神经元凋亡过程;AAP能降低caspase-3表达,减少神经元凋亡,有神经保护作用.  相似文献   

10.
虫草多糖对变性血红蛋白诱发的急性肾衰的防治作用研究   总被引：1，自引：0，他引：1  
目的探讨虫草多糖对大鼠静脉注射变性血蛋白诱发的急性肾衰的防治作用。方法将实验动物分为正常组,模型组,虫草多糖高、中、低三个剂量组和阳性组,观察治疗后大鼠的肾功能、血液生化指标、肾病理及肾脏指数的变化。结果虫草多糖组肾功能受损程度明显轻于模型组（P〈0．01）,肾脏病理损伤明显减轻,虫草多糖组与模型组比较肾脏指数有极显著差异（P〈0．01）。结论虫草多糖能够防治变性血蛋白诱发的急性肾功能衰竭,其机理可能与改善肾功能、纠正代谢紊乱、促进肾小管的修复与再生等作用有关。  相似文献   

11.
It has been reported that Ethaselen shows inhibitory effects on thioredoxin reductase (TrxR) activity and human tumor cell growth. In order to find an efficient way to reverse cisplatin resistance, we investigated the reversal effects of Ethaselen on cisplatin resistance in K562/cisplatin (CDDP) cells that were established by pulse-inducing human erythrocyte leukemic cell line K562, which are fivefold more resistant to cisplatin compared to K562 cells. The morphology and growth showed that the adhesion of K562/CDDP further decreased while the cell volume increased. The proliferation of K562/CDDP is strengthened. The antitumor activities in vitro were assessed by MTT (3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and combination index (CI), showing the significant synergic effects of cisplatin and Ethaselen. Focusing on apoptosis, a series of comparisons was made between K562 and K562/CDDP. Cisplatin induced higher reactive oxygen species (ROS) generation in K562 and subsequently induced the formation of mitochondrial permeability transition pores (PTPs). In addition, cisplatin increased the ratio of Bax to Bcl-2 in K562, which can influence the mitochondrial membrane permeability. PTP formation and mitochondrial membrane permeabilization eventually resulted in the release of cytochrome c and activation of the Caspase pathway. However, these effects were not clearly seen in K562/CDDP, which may be the reason for the acquired CDDP resistance. However, Ethaselen can induce a high level of ROS in K562/CDDP by TrxR activity inhibition and increased ratio of Bax to Bcl-2 in K562/CDDP by nuclear factor κB (NF-κB) suppression, which subsequently induces the release of cytochrome c in K562/CDDP. This response is partly responsible for the reversal of the cisplatin resistance in K562/CDDP cells.  相似文献   

12.
目的:研究复方金银花和茵陈五苓两种注射液对内毒素所致家兔肾衰中肾脏组织结构的保护作用。方法:将重量2.5±0.25kg的健康雄性家兔32只,随机分为对照组、模型组、复方金银花组和茵陈五苓组,每组8只。模型组、复方金银花组、茵陈五苓组家兔一次性静脉注射大肠杆菌O111B4内毒素生理盐水,剂量为100ug/kg。两保护组家兔注射内毒素24h后静脉注射剂量为100ug/kg的中药注射液。模型组家兔静脉注射同容积的生理盐水。对照组家兔静脉注射与内毒素溶液和中药注射剂等体积的生理盐水。静脉注射内毒素及生理盐水后第7h处死。取肾组织标本,Bouns液固定,石蜡切片,HE染色,显微观察并摄影。结果:模型组肾脏肾小体血管球肿胀,有血栓形成,肾小囊壁层内皮细胞脱落,肾小囊腔变小,肾小管内皮细胞脱落。复方金银花组、茵陈五苓组肾脏的肾小体血管球略有肿胀,肾小囊的内皮细胞较完整,肾小囊腔较对照组稍变小。结论:复方金银花与茵陈五苓对家兔因内毒素所致肾衰中肾脏组织结构有确实的保护作用。  相似文献   

13.
研究目的:在小鼠模型中利用吲哚美辛阻断COX-1/2通路,探讨非甾体类抗炎药对肾缺血再灌注损伤的保护作用。创新要点:非甾体类抗炎药被认为具有肾毒性,本研究首次在小鼠模型中探讨非甾体类抗炎药对肾缺血再灌注损伤的保护作用。研究方法:小鼠左侧肾蒂夹闭后,通过腹腔注射不同剂量的吲哚美辛,在肾缺血再灌注损伤24小时后,获取血液和肾脏标本。利用酶联免疫(ELISA)试剂盒测定血清肌酐和细胞因子浓度来评估肾功能,肾组织样本进行苏木精-伊红染色和免疫组化分析。重要结论:腹腔注射吲哚美辛5 mg/kg组的小鼠血清肌酐值与对照组相比显著降低,肾小管损伤也显著减轻(见图1和2);腹腔注射5和7 mg/kg吲哚美辛组的小鼠血清肾肿瘤坏死因子-α和白介素-6的浓度显著降低(见图3a和3b);腹腔注射3和5 mg/kg吲哚美辛组的小鼠血清血栓素B2与6-酮前列腺素F1α的比值明显降低(见图3c);腹腔注射5 mg/kg吲哚美辛组小鼠肾组织COX-1和COX-2染色较弱(见图4)。因此,吲哚美辛对小鼠肾缺血再灌注损伤的作用与其剂量相关,在某个特定的剂量范围内具有肾保护作用。吲哚美辛对小鼠肾缺血再灌注损伤的保护作用与阻断COX-1/2有关。  相似文献   

14.
ＩＮＴＲＯＤＵＣＴＩＯＮＴｈｅＮａ /Ｈ ｅｘｃｈａｎｇｅｒ (ＮＨＥ)ｉｓａｐＨ ｒｅｇｕｌａｔｏｒｙｐｒｏｔｅｉｎｐｒｅｓｅｎｔｉｎｔｈｅｐｌａｓｍａｍｅｍ ｂｒａｎｃｅｏｆｃａｒｄｉｏｍｙｏｃｙｔｅｓａｎｄｏｔｈｅｒｃｅｌｌｔｙｐｅｓ.ＡｌｔｈｏｕｇｈｓｅｖｅｒａｌｉｓｏｆｏｒｍｓｏｆＮＨＥｈａｖｅｂｅｅｎｄｅ ｃｒｉｂｅｄ,ｔｈｅｐｒｅｄｏｍｉｎａｎｔｉｓｏｆｏｒｍｉｎｔｈｅｈｅａｒｔｉｓｔｈｅｕｂｉｑｕｉｔｏｕｓＮＨＥ 1 ,ｗｈｉｃｈｕｎｄｅｒｃｅｎｔａｉｎｐｈｙｓｉｏｌｏｇｉｃａｌｃｏｎｄｉｔｉ…  相似文献   

15.
目的:观测尾加压素Ⅱ受体拮抗剂palosuran对阿霉素肾病大鼠尿中尾加压素Ⅱ(UrotensinⅡ;UⅡ)的影响,从而探究palosuran对微小病变肾病综合征(minimal change ne-phropathy syndrome;MCNS)的作用。方法:采用雄性Wistar大鼠80只,体重100±20g。随机选择其中10只做为健康组,其余70只大鼠尾静脉一次性注射阿霉素5mg/kg建立动物模型。注射后第7天检测大鼠24小时尿蛋白定量,若大鼠尿蛋白>30mg/24h者为MCNS模型成功,不合格者予以剔除。将合格的大鼠,随机分成2组,一组设为微小病变型肾病模型组,另一组在微小病变型肾病模型的基础上采用palosuran混入饲料中给药方法喂养,设为干预组。在实验第14、21、28天检测各组大鼠采用放射免疫法检测各组大鼠尿UⅡ的水平。结果:健康组大鼠尿UⅡ第14、21、28天检测值分别是1.46±0.18 ng/mL,1.52±0.12 ng/mL,1.54±0.43 ng/mL;模型组分别是2.49±0.11 ng/mL,4.48±0.19 ng/mL,6.56±0.27 ng/mL;干预组分别是1.95±0.1ng/mL,3.31±0.15 ng/mL,2.58±0.21 ng/mL。随着时间的延续,模型组大鼠尿UⅡ进行性升高(P<0.05),而palosuran对肾病大鼠尿UⅡ水平有明显影响,差异有显著统计意义(P<0.05)。结论:palosuran可能通过抑制UⅡ的作用而对微小病变肾病大鼠肾损害产生保护作用。  相似文献   

16.
目的：探讨口服吡喹酮的副反应及防治。方法：对口服吡喹酮致急性肾功衰的个案进行回顾性分析。结果：确认吡喹酮致急性肾功衰。结论：吡喹酮有导致肾功能损害的副作用。  相似文献   

17.
目的：观察天麻素对癫痫大鼠海马Caspase-3表达的影响及其脑保护作用。方法：120只健康成年雄性Wistar大鼠随机分为对照组、PTZ（戊四氮）组、VPA（丙戊酸钠）组、Gb（天麻素大剂量）组和Gs（天麻素小剂量）组（n=24）。对照组和PTZ组分别以生理盐水（4mL/kg·d）灌胃;VPA组给予丙戊酸20mg．kg^-1,Gb组和Gs组分别给予天麻素200mg．kg^-1和100mg．kg^-1;每天1次,连续7天。造模第一天,除对照组大鼠外,余者均腹腔注射戊四氮75mg／kg,记录动物行为学变化。于致痫后12h、2d、5d和7d相应时间点取材,制备脑标本,免疫细胞化学术检测caspase-3表达。结果：致痫后12h,P11Z组Caspase-3有微量表达,其余各组几乎无表达;2—7d。PTZ组Caspase-3表达增加。与PTZ组比较,Gb组、Gs组及VPA组Caspase-3阳性表达降低,差异显著（P〈0．05）;与VPA组比较,Gb组和Gs组Caspase-3表达无显著差异（P〉0．05）。结论：天麻素能降低致痫大鼠海马神经元Caspase-3表达;可能通过抑制神经元凋亡发挥脑保护作用。  相似文献   

18.
目的:观察甘油致急性肾功能衰竭(ARF)家兔自由基的变化,探讨自由基损伤在ARF发生中的作用及其意义.方法:30只家兔随机分为两组:50%甘油(10ml/kg.bw)肌肉注射复制家兔ARF模型,等量生理盐水代替甘油作为对照组(n均=15).分别应用改良TBA微量法、黄嘌呤氧化酶法测定血清及肾脏组织匀浆的丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性的变化.结果:ARF组血清及肾脏组织匀浆的MDA水平高于对照组(P＜0.01),SOD活性显著低于对照组(P＜0.01).结论:自由基损伤在甘油致家兔ARF过程中具有重要作用.  相似文献   

19.
Objective:To report a case of Wernicke encephalopathy in the early stage after surgery.Methods:A nonalcoholic female patient with hepatitis B-related cirrhosis and hypersplenism underwent splenectomy in a local hospital.No surgical complications occurred and the patient recovered well.However,on the eighth postoperative day she developed psychiatric and neurological disturbance without an obvious cause.She was then admitted to our hospital.Brain magnetic resonance imaging(MRI) with FLAIR T2 showed symmetric high-signal intensities in the periaqueductal area of the midbrain,which were consistent with Wernicke encephalopathy.She was thus given in-tramuscular thiamine immediately.Results:After the administration of thiamine,the patient's confused mental state resolved within 3 d,and her dystaxia gradually improved over the next 5 d.The brain MRI with FLAIR T2 was re-examined one month after the episode,and showed nearly complete resolution of the previously abnormal signal intensities in the periaqueductal area of the midbrain.Conclusion:Physicians should be aware of the possibility of acute Wernicke encephalopathy,especially in patients with liver dysfunction.  相似文献   

20.
建立了检测1640培养液中顺铂含量的火焰原子吸收光谱实验方法,并用该方法来检测人白血病细胞K562经10μg/mL顺铂孵育8 h后,细胞外液的顺铂含量.具体方法为:将含有顺铂的培养液加热干燥后用含有释放剂的无机酸溶剂溶解,火焰原子吸收光谱法测定铂的含量.对无机酸和释放剂进行了筛选,确定了最佳测定条件并检测了上述实验条件下细胞外液中的顺铂含量.结果显示,含顺铂的培养液或细胞外液加热干燥后,可用体积分数为1%HNO3溶液完全溶解,在溶解过程中加入质量分数为1%的La(NO3)3,可使铂成分获得良好的释放效果.K562细胞经10μg/mL顺铂孵育8 h可致细胞活性显著下降(P0.05),此时约6.2%顺铂进入胞内.与传统顺铂检测方法相比,文中的制样方法可使样品不经灰化即可有效检测肿瘤细胞对顺铂的吸收量.  相似文献   

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