Therapeutic Effect of Intragastric Administration of Jiangtang Shuxin Recipe Suspension on Diabetic Heart Failure in Rats and Its Mechanism

[Objectives]To observe the therapeutic effect of intragastric administration of Jiangtang Shuxin recipe on diabetic heart failure(DHF)in rats and to explore its mechanism.[Methods]Fifty SD rats were randomly divided into five groups,with 10 rats in each group.DHF models were prepared in the low-dose group,high-dose group,Western medicine group,and model group except the control group.Rats in the low-dose and high-dose groups were given 1.0 and 1.5 g/(kg·d)Jiangtang Shuxin recipe suspension by gavage,respectively.Rats in the Western medicine group were given gliquidone and benazepril by gavage for 2 months,and were fed with high-fat diet.Rats in the control group were fed with ordinary diet.Fasting blood glucose(FBG),serum triglyceride(TG),low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C),C-reactive protein(CRP),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),creatine kinase isoenzyme(CK-MB),lactate dehydrogenase(LDH),pathological morphology of myocardial tissue,NF-κB p65 protein and IκBαprotein were compared among groups.[Results]Compared with the control group,the levels of FBG,serum TG,LDL-C,CRP,IL-6,TNF-α,CK-MB and LDH increased,while the level of serum HDL-C decreased.The myocardial tissue was seriously damaged,and the expression of NF-κB p65 protein increased,while the expression of IκBαprotein decreased in the other four gruops(all P<0.05).Compared with the model group,the levels of FBG,serum TG,LDL-C,CRP,IL-6,TNF-α,CK-MB and LDH decreased,while the serum HDL-C level increased.The myocardial tissue damage was alleviated,and the expression of NF-κB p65 protein decreased,while the expression of IκBαprotein increased in the low-dose group,high-dose group and Western medicine group(all P<0.05).Compared with the Western medicine group,the levels of FBG,serum TG,LDL-C,CRP,IL-6,TNF-α,CK-MB and LDH decreased,and the level of serum HDL-C increased in the high-dose group(all P<0.05).[Conclusions]Jiangtang Shuxin recipe has a therapeutic effect on DHF in rats,with the best effect in the high-dose group.It can not only alleviate high glucose and high fat state,but also reduce myocardial injury and inflammation,and improve the pathological morphology of myocardial cells.The mechanism may be related to its inhibition of NF-кB signaling pathway.

Dan Huang Ming Mu Recipe Suppresses the Progression of Streptozotocin-induced Diabetic Retinopathy After Retinal Laser Photocoagulation in Brown Norway Rats via Down-regulating Vascular Endothelial Growth Factor and Up-regulating Pigment Epithelium-derived

Objective To analyze the effects of Dan Huang Ming Mu Recipe(DHMMR)(a pharmaceutical preparation from herbs and having the function of replenishing vital essence,removing heat,promoting blood circulation and excreting pathogenic water) on diabetic retinopathy(DR) after retinal laser photocoagulation through regulating the expression of vascular endothelial growth factor(VEGF) and pigment epithelium-derived factor(PEDF).Methods Forty male Brown Norway(BN) rats were randomly divided into blank group(group A,10 BN rats) and model group(30 BN rats).DR models were induced by 40 mg/kg streptozotocin(STZ) and the body weight and blood glucose of rats were monitored.After 12-week injection,fluorescein fundus angiography(FFA) and histopathological examination were detected to confirm the successful establishment of DR models.Subsequently,the right eyes of model group rats were conducted retinal laser photocoagulation with the left eyes having no retinal laser photocoagulation and rats of the model group were randomly divided into group B(the model control group),group C(the positive control group),and group D(the DHMMR group),with 10 rats in each group.Rats of the group A and the group B were given vehicle,and the group C were given calcium dobesilate suspension by gavage,and the group D were given DHMMR by gavage.After 4-week gavage,FFA was carried out to observe the fundus microvascular change.Then,the rats were sacrificed to do histopathological examinations and the serum levels of P-selectin,cAMP,cGMP,and the relative expression of the protein of VEGF and PEDF in retina were detected.Results After 12-week STZ injection,the blood glucose of the model group were pronouncedly higher than the blank group(P < 0.01).Fundus micro-hemangioma changes were observed in the rats of the model group through FFA,and the rats of the blank group did not see any changes.The pictures of HE staining showed that the retinal structure of the model group was more disordered than the blank group.After 4-week gavage,treatments with DHMMR showed dramatic reduction of serum levels of Pselectin,cAMP and cGMP compared with the group B(P < 0.01).FFA and histopathological examinations of DHMMR-treated rats revealed significantly suppression of retinal edema,fundus microvascular destruction and retinal destruction distinguishing from the group B.And the relative expression of VEGF protein of the group D and the group A was markedly lower than that of the group B(P < 0.01).The relative expression of PEDF protein of the group D and the group A was dramatically higher than that of the group B to the contrary(P < 0.01).Conclusions DHMMR demonstrates pronounced suppressive effects on the progression of DR after retinal laser photocoagulation,through down-regulating VEGF and upregulating PEDF.

Progress in experimental models to investigate the in vivo and in vitro antidiabetic activity of drugs

Diabetes mellitus is one of the world's most prevalent and complex metabolic disorders,and it is a rapidly growing global public health issue.It is characterized by hyperglycemia,a condition involving a high blood glucose level brought on by deficiencies in insulin secretion,decreased activity of insulin,or both.Prolonged effects of diabetes include cardiovascular problems,retinopathy,neuropathy,nephropathy,and vascular alterations in both macro-and micro-blood vessels.In vivo and in vitro models have always been important for investigating and characterizing disease pathogenesis,identifying targets,and reviewing novel treatment options and medications.Fully understanding these models is crucial for the researchers so this review summarizes the different experimental in vivo and in vitro model options used to study diabetes and its consequences.The most popular in vivo studies involves the small animal models,such as rodent models,chemically induced diabetogens like streptozotocin and alloxan,and the possibility of deleting or overexpressing a specific gene by knockout and transgenic technologies on these animals.Other models include virally induced models,diet/nutrition induced diabetic animals,surgically induced models or pancreatectomy models,and non-obese models.Large animals or non-rodent models like porcine(pig),canine(dog),nonhuman primate,and Zebrafish models are also outlined.The in vitro models discussed are murine and human beta-cell lines and pancreatic islets,human stem cells,and organoid cultures.The other enzymatic in vitro tests to assess diabetes include assay of amylase inhibition and inhibition ofα-glucosidase activity.

Clinical efficacy of angina pectoris after pci in patients with coronary heart disease complicated with type 2 diabetes by Yiqi Yangyin and Huatan Tongluo recipe

Objective:To evaluate the clinical efficacy of Yiqi Yangyin and Huatan Tongluo Recipe in improving the symptoms of angina pectoris and cardiac function in patients with coronary heart disease complicated with type 2 diabetes after PCI.Methods Sixty-two patients with coronary heart disease complicated with type 2 diabetes after PCI were randomly divided into treatment group and control group,with 31 patients in each group.Both groups were treated with western medicine.The treatment group added Yiqi Yangyin and Huayu Tongluo Recipe granules.The changes of metabolic equivalent(METs),angina symptoms,TCM symptoms,BNP,hypersensitive C-reactive protein(hs-CRP),Interleukin-6(IL-6),Tumor necrosis factor-(TNF-α)and left ventricular ejection fraction(LVEF)were analyzed after 1 course of treatment and Corrected TIMI Frame Count(CTFC)after six month.Results The improvement of METS and LVEF in the treatment group was better than that in the control group(P<0.05);the improvement of BNP,hs-CRP,IL-6,TNF-αand CTFC in the treatment group was better than that in the control group;the curative effect of angina pectoris in the treatment group was better than that in the control group;the effective rate of TCM syndrome improvement in the treatment group was better than that in the control group.Conclusion Yiqi Yangyin and Huatan Tongluo Recipe can effectively alleviate angina pectoris symptoms in patients with coronary heart disease complicated with type 2 diabetes after PCI,suggesting cardiac function,inhibiting inflammatory response,and improving microcirculation disturbance.

CD47 decline in pancreatic islet cells promotes macrophage-mediated phagocytosis in type Ⅰ diabetes

BACKGROUND Type Ⅰ diabetes(T1D)is characterized by insulin loss caused by inflammatory cells that excessively infiltrate and destroy the pancreas,resulting in dysregulation of tissue homeostasis,mechanobiological properties,and the immune response.The streptozotocin(STZ)-induced mouse model exhibits multiple features of human T1D and enables mechanistic analysis of disease progression.However,the relationship between the mechanochemical signaling regulation of STZ-induced T1D and macrophage migration and phagocytosis is unclear.AIM To study the mechanochemical regulation of STZ-induced macrophage response on pancreatic beta islet cells to gain a clearer understanding of T1D.METHODS We performed experiments using different methods.We stimulated isolated pancreatic beta islet cells with STZ and then tested the macrophage migration and phagocytosis.RESULTS In this study,we discovered that the integrin-associated surface factor CD47 played a critical role in immune defense in the STZ-induced T1D model by preventing pancreatic beta islet inflammation.In comparison with healthy mice,STZ-treated mice showed decreased levels of CD47 on islet cells and reduced interaction of CD47 with signal regulatory proteinα(SIRPα),which negatively regulates macrophage-mediated phagocytosis.This resulted in weakened islet cell immune defense and promoted macrophage migration and phagocytosis of target inflammatory cells.Moreover,lipopolysaccharide-activated human acute monocytic leukemia THP-1 cells also exhibited enhanced phagocytosis in the STZ-treated islets,and the aggressive attack of the inflammatory islets correlated with impaired CD47-SIRPαinteractions.In addition,CD47 overexpression rescued the pre-labeled targeted cells.CONCLUSION This study indicates that CD47 deficiency promotes the migration and phagocytosis of macrophages and provides mechanistic insights into T1D by associating the interactions between membrane structures and inflammatory disease progression.

8-isoPGF2α、Metrnl、LC3B-Ⅱ/LC3B-Ⅰ与T2MD患者血糖在目标范围内时间的相关性及预测糖尿病周围神经病变的价值

目的探讨8-异前列腺素F2α(8-isoPGF2α)、镍纹样蛋白(Metrnl)、微管相关蛋白3B-Ⅱ(LC3B-Ⅱ)/微管相关蛋白-Ⅰ(LC3B-Ⅰ)与2型糖尿病(T2MD)患者血糖在目标范围内时间(TIR)的相关性及对糖尿病周围神经病变(DPN)预测价值。方法选取2020年5月至2022年10月新乡医学院第一附属医院收治的187例T2DM患者进行前瞻性研究,根据是否合并DPN分为DPN组(n=48)和无DPN组(n=139)。比较两组患者及根据TIR四分位数分组的患者8-isoPGF2α、Metrnl、LC3B-Ⅱ/LC3B-Ⅰ水平,采用Pearson相关性分析8-isoPGF2α、Metrnl、LC3B-Ⅱ/LC3B-Ⅰ与TIR相关性,采用多因素Logistic回归分析DPN的相关影响因素;绘制受试者工作特征曲线(ROC)评价8-isoPGF2α、Metrnl、LC3B-Ⅱ预测DPN的价值。结果DPN组患者的TIR为(51.43±7.68)%,明显低于无DPN组的(56.94±8.12)%,差异有统计学意义(P<0.05);DPN组患者的8-isoPGF2α、Metrnl分别为(162.78±51.33)pg/mL、(259.18±74.42)pg/mL,明显高于无DPN组的(129.56±43.00)pg/mL、(208.37±65.61)pg/mL,LC3B-Ⅱ/LC3B-Ⅰ为0.89±0.27,明显低于无DPN组的1.15±0.31,差异均有统计学意义(P<0.05);根据TIR第25、50、75百分位数将全部患者分为Q1~Q4四组,8-isoPGF2α、Metrnl在Q4组最低,LC3B-Ⅱ/LC3B-Ⅰ在Q4组最高;8-isoPGF2α、Metrnl随着TIR降低逐渐升高,LC3B-Ⅱ/LC3B-Ⅰ随着TIR降低而降低,四组间比较差异均有统计学意义(P<0.05);Pearson相关性分析结果显示,8-isoPGF2α、Metrnl与TIR呈显著负相关(r=-0.786、-0.665,P<0.01),LC3B-Ⅱ/LC3B-Ⅰ与TIR呈显著正相关(r=0.711,P<0.01);多因素Logistic回归分析结果显示,TIR、LC3B-Ⅱ/LC3B-Ⅰ是DPN的独立相关保护因素(P<0.05),8-isoPGF2α、Metrnl是DPN的独立相关危险因素(P<0.05);ROC分析结果显示,单一指标中,Metrnl预测DPN的AUC最大(0.830),特异度最高(87.05%),8-isoPGF2α+Metrnl+LC3B-Ⅱ预测DPN的AUC为0.923(95%CI:0.875~0.957),大于Metrnl,预测敏感度为87.50%,特异度为85.61%(P<0.05)。结论8-isoPGF2α、Metrnl、LC3B-Ⅱ/LC3B-Ⅰ与T2MD患者TIR有关,均是患者并发DPN的预警因素。联合检测三者能为临床分层管理和早期识别DPN高风险人群提供参考。

生肌化瘀方及其拆方对大鼠创面成纤维细胞Ⅰ、Ⅲ型胶原合成的影响

目的 :探讨生肌化瘀方及其拆方促进创面修复 (呈皮肤修复 )的作用机理。方法 :采用体外培养创面肉芽组织成纤维细胞 ,以乳鼠皮肤成纤维细胞作对照 ,分别加入生肌方、化瘀方及生肌化瘀方大、小剂量药物血清 ,运用细胞化学ABC法检测成纤维细胞Ⅰ、Ⅲ型胶原的含量。结果 :生肌方能够提高创面成纤维细胞Ⅰ、Ⅲ型胶原含量 ,且均高于模型组 (P <0 0 1) ;化瘀方能够降低创面成纤维细胞Ⅰ、Ⅲ型胶原含量 ,且低于模型组 (P <0 0 1) ;生肌化瘀方大、小剂量组Ⅰ、Ⅲ型胶原含量与正常组比较差异均无显著性 (P >0 0 5 )。结论 :生肌化瘀方能够促进创面修复 ,其可能的作用机理是通过调节Ⅰ、Ⅲ型胶原的比值来调控Ⅰ。

生肌化瘀方及其拆方对大鼠创面修复早期肉芽组织中Ⅰ、Ⅲ型胶原的影响

目的:探讨生肌化瘀方及其拆方对创面修复早期Ⅰ、Ⅲ型胶原的影响。方法:将24 只清洁级雄性SD大鼠随机分为4组:生肌化瘀方组、生肌方组、化瘀方组和模型组。以大鼠皮肤全层缺损创面为模型,采用免疫组化和图像分析相结合的方法,观察各组大鼠创面修复早期肉芽组织中Ⅰ、Ⅲ型胶原的变化。结果:在创面修复的第3 天,生肌方组和生肌化瘀方组的Ⅰ型胶原水平均高于模型组,化瘀方组则低于模型组(P <0.05);生肌方组、化瘀方组和生肌化瘀方组的Ⅲ型胶原水平均低于模型组(P<0.05),以化瘀方组更为明显;在创面修复的第7 天,生肌方组、生肌化瘀方组的Ⅰ型胶原水平均低于模型组(P<0.05);生肌方组和化瘀方组的Ⅲ型胶原水平均高于模型组(P<0.05)。结论:祛瘀生肌法可以促进大鼠创面修复,减少瘢痕形成。

实验性糖尿病早期大鼠组织IGF-Ⅰ基因的研究

目的 探讨实验性糖尿病早期大鼠组织胰岛素样生长因子 - (IGF- )基因的表达及意义。方法 四氧嘧啶(alloxan)诱发大鼠糖尿病模型后 2周时 ,用逆转录 (RT) - PCR分析了肝脏及坐骨神经组织 IGF- 基因表达 :m RNA含量。结果 2种组织的 IGF- m RNA均下降 ,程度因糖尿病严重状态而异 ,且出现在神经电生理异常之前。结论 糖尿病早期 IGF- m

补肾益气活血方对宫内发育迟缓胎鼠肝脏IGF-Ⅰ表达的影响

目的 观察补肾益气活血方对宫内发育迟缓 (intrauterine growth retardation,IU GR)胎鼠肝脏胰岛素样生长因子 - 1(insulin like growth factor- ,IGF- )基因在转录和翻译水平上的影响 ,探讨其防治 IU GR的作用机制。方法 采用被动吸烟法复制胎鼠 IU GR模型 ,分为正常对照组、 IU GR组、 IUGR精氨酸治疗组 (精氨酸组 )、 IU GR补肾益气活血方治疗组 (中药组 )。采用 Northern blot和免疫组织化学的方法分别检测胎鼠肝脏 IGF- m RNA和蛋白的表达。结果 IUGR组 IGF- m RNA及蛋白表达水平与对照组比较明显下调 (P<0 .0 1) ,而精氨酸组和中药组两者表达水平较 IUGR组有所增加 ,其中 ,中药组 IGF- 的表达强度高于精氨酸组 (P<0 .0 5 ) ,接近正常组 (P>0 .0 5 )。结论补肾益气活血方可能通过直接 (或间接 )促进 IGF- 的合成和分泌 ,或者防止某些致病因素对 IGF- 基因表达细胞信息传导途径的阻断而起到防治

血管紧张素Ⅱ及氯沙坦对糖尿病大鼠心肌成纤维细胞α_1(Ⅰ)前胶原mRNA和蛋白表达的影响

目的 探讨血管紧张素Ⅱ(ATⅡ)及其1 型受体阻断剂氯沙坦对糖尿病动物模型心肌成纤维细胞α1(Ⅰ)前胶原mRNA和蛋白表达的作用。 方法 用链脲佐菌素制备糖尿病大鼠模型,饲养12周后分离心肌成纤维细胞进行原代培养。分别将一定浓度的AT Ⅱ(10-9~10-7 mmol/L),和ATⅡ10-7 mmol/L加上不同浓度ATⅡ受体阻滞剂氯沙坦(10-7~10-5 mmol/L)加入细胞培养液中刺激48 h,分别采用逆转录聚合酶链反应(RT-PCR)及Western 印迹方法检测大鼠心肌成纤维细胞α1(Ⅰ)前胶原的mRNA及蛋白表达。 结果 体外成功地培养糖尿病心肌成纤维细胞,并经免疫组化染色结果证实。经ATⅡ刺激48 h后,α1(Ⅰ)前胶原mRNA和蛋白表达量明显增高,增高程度与ATⅡ浓度呈正比;加入氯沙坦后,前胶原mRNA和蛋白表达量较单用ATⅡ组下降,也呈浓度依赖性。 结论 ATⅡ可促进糖尿病大鼠心肌成纤维细胞的胶原合成,可能在糖尿病大鼠心肌纤维化倾向中起重要作用,该作用可能主要通过ATⅡ1型受体介导完成。

牛初乳短链IGF-Ⅰ对STZ糖尿病大鼠心肌细胞Ca^(2+)的影响

为了解牛初乳短键类胰岛素样生长因子-I（IGF－I）对糖尿病大鼠心肌细胞Ca2+的影响，我们用牛初乳短键IGF－I治疗涟豚佐菌素（STZ）糖尿病大鼠。利用原子光谱吸收法测定发现STZ糖尿病大鼠心肌细胞Ca2+的含量明显高于正常对照组[分别为（54．5±9．6）及（24．4±80）μg/g心肌]；牛初乳短键IGF－I口服（15μg／kg体重）或腹腔注射（250ng/kg体重）治疗5周后的糖尿病大鼠血清IGF一I浓度有显著增加，心肌细胞Ca2+含量显著降低［分别为（37．3±14．5）及（27．5±9．7）μg／g心肌]，达正常水平。提示牛初乳短链IGF－I能逆转糖尿病时心肌细胞Ca2+超载现象，为糖尿病心肌病变提供了一种可能的预防措施。

胰岛素样生长因子Ⅰ对高糖条件下成骨细胞骨形成的影响

目的:研究胰岛素样生长因子I对高糖条件下成骨细胞骨形成的影响,探讨胰岛素样生长因子I对糖尿病性骨病的作用机制。方法:离体实验通过对细胞增殖和矿化的检测,从细胞分子水平评价胰岛素样生长因子I对高糖环境下成骨细胞的作用。体内实验诱导1型糖尿病大鼠动物模型,分别给予胰岛素(6～8U/d)和胰岛素样生长因子I(30μg/kg.d)治疗,通过X线、组织切片HE染色和四环素双标记的方法观察牙槽骨改建情况。结果:离体实验的结果显示胰岛素样生长因子I可减少高浓度葡萄糖引起的成骨细胞的异常增殖,促进钙沉积和矿化结节的形成。体内实验研究显示与正常组相比,糖尿病大鼠拔牙创骨愈合减慢,骨形成减少,牙槽骨高度和牙槽骨骨形成率显著降低。胰岛素样生长因子I的治疗不仅能控制糖尿病大鼠的血糖保持在正常范围内,还可以增加牙槽骨高度和提高骨形成率。结论:高浓度葡萄糖导致糖尿病大鼠拔牙后骨形成减少、牙槽骨高度降低等病理改变;胰岛素样生长因子I可以促进糖尿病状态下成骨细胞骨形成和矿化,有利于糖尿病大鼠拔牙后骨创愈合和新骨形成。

补肾方药对骨质疏松大鼠骨基质Ⅰ型胶原表达的影响

目的 :探讨补肾方药预防糖皮质激素诱导大鼠骨质疏松发生的机制。方法 :通过肌肉注射地塞米松造成骨质疏松模型 ,观察补肾中药对骨密度的影响 ,从骨骼中提取 m RNA,采用 RT- PC方法对 型胶原m RNA进行半定量。结果 :病理组大鼠的骨密度及骨骼中 型胶原 m RNA的表达明显降低 ( P<0 .0 5) ,而补肾方药组的骨密度及 型胶原 m RNA的表达明显高于地塞米松组 ( P<0 .0 5)。结论 :地塞米松抑制 型胶原 m RNA在骨骼的表达 ,补肾方药可通过提高 型胶原 m RNA在骨的表达而预防骨质疏松的发生。

抗纤复方药物血清对HSC-LI90细胞Ⅰ型、Ⅳ型前胶原和基质金属蛋白酶及其组织抑制因子-1基因表达的影响

目的 :探讨抗纤复方药物血清对肝星形细胞 (HSC)LI90细胞 (HSC LI90 )Ⅰ型、Ⅳ型前胶原和基质金属蛋白酶 (MMPs)及其组织抑制因子 (TIMP 1)基因表达的影响。方法 :以 0 5、2 0、4 0 g/kg等不同剂量抗纤复方灌胃大鼠 ,制备药物血清 ,作用于HSC LI90细胞 4 8h ,应用Northern印迹杂交的方法 ,检测Ⅰ型、Ⅳ型前胶原、基质金属蛋白酶 2 (MMP 2 )及膜型基质金属蛋白酶 (MT1 MMP)及其组织抑制因子(TIMP 1)基因的表达 ,并用酶图法检测基质金属蛋白酶 2的活性。结果 :(1)抗纤复方不同浓度药物血清能抑制HSC LI90细胞Ⅰ型、Ⅳ型前胶原及其组织抑制因子TIMP 1的基因表达 (P <0 0 5或P <0 0 1) ;(2 )能增加膜型基质金属蛋白酶基因表达 (P <0 0 1) ;(3)对基质金属蛋白酶 2基因表达及活性无影响 (P >0 0 5 )。结论 :(1)抗纤复方具有抗肝纤维化作用 ;(2 )抗纤复方抑制HSC LI90细胞TIMP 1基因表达水平 ,促进胶原降解 ,可能是抗肝纤维化的作用机制之一。

黄芪对糖尿病足溃疡处成纤维细胞合成Ⅰ、Ⅲ型胶原的影响

目的探讨黄芪对糖尿病足溃疡处成纤维细胞Ⅰ、Ⅲ型胶原mRNA及Ⅰ、Ⅲ型胶原分泌的影响。方法用含/未含黄芪的培养液培养糖尿病足溃疡处成纤维细胞,RT-PCR检测Ⅰ、Ⅲ型胶原mRNA表达,放免法检测培养上清液中Ⅰ、Ⅲ型胶原含量。结果用含黄芪的培养液培养的糖尿病足溃疡处成纤维细胞Ⅰ、Ⅲ型胶原mRNA表达及培养上清液中Ⅰ、Ⅲ型胶原含量高于未含黄芪的培养液培养的细胞,且差异有统计学意义(P<0.05)。结论黄芪能上调糖尿病足溃疡处成纤维细胞Ⅰ、Ⅲ型胶原mRNA表达和促进Ⅰ、Ⅲ型胶原的合成。

中药热熨Ⅰ号方治疗阳虚寒凝型膝关节骨性关节炎的临床疗效观察

目的观察中药热熨Ⅰ号方治疗阳虚寒凝型膝关节骨性关节炎的临床疗效。方法将符合入选标准的门诊患者89例随机分为治疗组和对照组,其中治疗组46例以中药热熨Ⅰ号方于膝关节局部熨敷患膝,对照组43例应用双氯芬酸钠乳膏外用涂擦患处进行治疗。在治疗后第2、4周对患者症状、体征积分、关节炎影响指数和安全性指标进行评估。结果 2组治疗后4周总疗效比较,治疗组总有效率为86.7%,对照组总有效率为90.7%,2组间差别无统计学意义(P>0.05)。2组治疗后2、4周症状、体征、关节炎影响指数以及单症状、单体征等积分自身比较,差别均有统计学意义(P<0.05)。结论热熨Ⅰ号方可明显缓解和改善膝关节骨性关节炎患者的症状和体征,改善关节功能,从而促进和提高患者的日常活动以及生活质量,但其作用机制及远期疗效尚有待于通过进一步动物实验研究和临床观察来验证和阐明。

补肾活血方与PRP对Ⅰ型胶原活性和表达的影响

目的:观察补肾活血方与富血小板血浆(PRP)对共培养体系中Ⅰ型胶原活性和表达的影响。方法:取腰椎间盘退变行髓核摘除手术患者的皮下脂肪组织及退变髓核组织,运用多次酶消化法原代分离、培养,建立ADSCs/NPCs共培养体系。纳入腰椎间盘退变患者,连续服用补肾活血方2周,分别于初次服药前和末次服药后1 h抽取静脉血各50 mL,采用二次离心法制备富血小板血浆,以不同血浆干预培养。实验共分为5组:富血小板血浆组(PRP)、贫血小板血浆组(PPP)、含药富血小板血浆组(M-PRP)和含药贫血小板血浆组(M-PPP)、胎牛血清组(FBS)。倒置显微镜下观察各组细胞的形态变化;采用细胞免疫荧光法检测Ⅰ型胶原活性变化;干预培养2周后采用RT-PCR法检测细胞COL1A1基因表达水平。结果:本研究发现经过补肾活血方和PRP分组干预后的结果显示,与其余组别相比,M-PRP组及PRP组细胞轮廓更为清晰、折光度更好,两组之间无明显差异。细胞免疫荧光染色结果显示,PRP组和M-PRP组细胞数量较多,但单个细胞的染色强度明显低于FBS组。RT-PCR结果显示,PPP组、PRP组、M-PRP组和M-PPP组COL1A1 mRNA表达均显著下调(P<0.05)。结论:补肾活血方联合富血小板血浆组可在一定程度上降低Ⅰ型胶原活性,抑制其表达功能。

糖尿病视网膜病变患者血清β_2-糖蛋白Ⅰ的表达

目的探讨血清β2-糖蛋白Ⅰ(beta2-glycoproteinⅠ,β2-GPⅠ)在不同时期糖尿病视网膜病变(diabetic retinopathy,DR)患者中的变化,了解血清β2-GPⅠ与DR的关系。方法收集60例2型糖尿病患者血清标本,将其分为3组:20例无明显DR(no-DR,NDR)患者为NDR组;20例非增生性DR(non-proliferative DR,NPDR)患者为NPDR组;20例增生性DR(proliferative DR,PDR)患者为PDR组。同时收集20例健康人血清为正常对照(normal control,NC)组。应用Westernblot方法,对各组随机抽取的4份血清样本中β2-GPⅠ水平进行分析。结果β2-GPⅠ水平在NPDR组、PDR组大量表达,在NDR组中量表达,在NC组少量表达。NC组、NDR组、NPDR组和PDR组各条带面积平均光密度值,分别为(440564.9±66597.4)mm-2、(655561.6±85640.8)mm-2、(859969.7±85461.0)mm-2、(954887.4±125764.4)mm-2。与NC组比较,β2-GPⅠ水平在NDR组、NPDR组、PDR组显著升高,差异均有统计学意义(均为P<0.01);与NDR组比较,β2-GPⅠ水平在NPDR组、PDR组显著升高,差异均有统计学意义(均为P<0.01);与NPDR组比较,PDR组无明显升高,差异无统计学意义(P>0.05)。结论在DR发生过程中,血清β2-GPⅠ水平上调,β2-GPⅠ可能具有潜在的早期诊断DR的价值。

Ⅱ型糖尿病人血浆中内皮素－Ⅰ含量增值的临床意义

用放射免疫法观察了４０例Ⅱ型糖尿病人外周血浆中内皮素的含量及与病程、年龄、空腹血糖（ＦＢＧ）、糖化血红蛋白（ＨｂＡ１）、Ｃ肽、血压的相关关系，并比较了伴和不伴视网膜病变或心脏病变的糖尿病人血浆内皮素水平的不同，其中２０例糖尿病人血浆内皮素含量较年龄、性别匹配的正常对照者明显升高。结果提示：内皮素－Ⅰ可能与糖尿病的慢性血管并发症有密切的联系。