活血消癥颗粒治疗子宫肌瘤400例临床研究

目的观察活血消癥颗粒对子宫肌瘤的缩瘤效果及对临床证候群的改善情况。方法400例子宫肌瘤患者随机分为治疗组300例口服活血消癥颗粒剂,对照组100例口服米非司酮。观察两组治疗后总疗效、症状改善情况、子宫体积及肌瘤体积变化情况。结果活血消癥颗粒组总有效率(92.3%)、子宫体积及肌瘤体积与对照组比较无统计学意义(P>0.05),但在改善症状及减少肌瘤复发等方面明显优于米非司酮(P<0.05),且无不良反应。结论活血消癥颗粒与米非司酮对子宫肌瘤均有较好的治疗作用,但活血消癥颗粒剂能有效改善临床症状,且缩瘤效果稳定,不良反应小,是治疗子宫肌瘤的有效方药,尤其在治疗直径<3cm肌瘤方面疗效明显。

活血消癥胶囊与化瘀止痛胶囊分期治疗子宫腺肌病临床研究

目的观察活血消癥胶囊与化瘀止痛胶囊分期治疗子宫腺肌病的临床疗效及作用机理。方法将68例患者随机分为治疗组(37例,口服活血消癥胶囊与化瘀止痛胶囊)与对照组(31例,口服米非司酮),比较两组痛经、子宫大小及血清CA125、血液流变性、ET-1的变化。结果治疗后两组痛经症状明显改善,两组疗效相近;两组治疗后子宫体积明显缩小、血清CA125值明显降低;治疗组治疗后血液流变学指标和ET-1水平改善明显。结论活血消癥胶囊与化瘀止痛胶囊分期治疗子宫腺肌病能缓解痛经症状、缩小增大的子宫,其机理可能与降低血浆中ET-1含量,改善体内血液高凝状态,促进血液微循环,使局部异位内膜萎缩吸收有关。

加减血汤抗小鼠移植性肿瘤的实验研究

研究加减血汤体内抗移植性肿瘤的作用及其参与肿瘤的凋亡、侵袭、转移等恶性生物学行为,为加减血汤的临床应用提供理论依据。方法:加减血汤醇提液灌饲接种过人胃癌SGC-7901细胞的荷瘤小鼠,并通过测定其抑瘤率、瘤体免疫组化检测VEGF、HIF-1α、CD31蛋白表达来进一步探讨其抗瘤活性作用。结果:不同剂量加减血汤具有抗人胃癌SGC-7901移植性肿瘤的作用,抑瘤率达60%、37%、31%,同时可以下调VEGF、HIF-1α、CD31蛋白表达。结论:加减血汤具有较强的抗肿瘤的作用,可能与下调VEGF、HIF-1α、CD31蛋白表达有关。

轻中型基底节区脑出血使用活血化瘀治疗临床观察

目的 观察脑基底节区出血早期使用活血化瘀治疗的效果。方法 把64例病人随机分为三七总甙治疗组及对照组进行治疗，对其血肿吸收，神经功能缺损评分及Barthel指数评估进行比较，采用t检验。结果 治疗组在血肿吸收，NDF评分及Barthel指数评估均优于对照组。结论 早期使用活血化瘀治疗脑出血，能改善残障功能，提高生活质量。

200例乳房囊性增生症甲襞微循环观察

本文对200例乳房囊性增生症进行了微循环观察,结果发现均有不同程度的微循环障碍存在,主要变化为:管周渗出197例,占98.5％;袢顶瘀血184例,占92％;流速变慢141例,占70.5％;管袢轮廓模糊135例,占67.5％;其余变化依次为红细胞聚集,管袢数目减少,长度下降,畸形增多,管径纤细。以上表明本病有不同程度的瘀血症存在。可见微循环现察对中医瘀血症的研究有积极意义。

中西结合治疗慢性输卵管炎39例临床观察

目的探讨中西结合治疗慢性输卵管炎的临床疗效，研究中药活血消瘢汤等的临床应用。方法观察患者78例分为治疗组和对照组，对照组用常规西药消炎加超短波治疗，治疗组在对照组的基础上加自拟中药活血消症汤内服外敷和银翘红酱汤浓煎保留灌肠；均治疗1～3个疗程后观察治疗效果。结果治疗组治愈率56．41％，治疗有效率87．28％；对照组治愈率30．77％，治疗有效率64．10％。两组治愈率及治疗总有效率对比均有显著性差异(P<0．05)。结论中药活血消症汤内服外敷加银翘红酱汤保留灌肠可明显提高慢性输卵管炎的治疗效果，中西结合治疗慢性输卵管炎是值得推广的较好的办法。

Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway:an in vitro study

Accumulating evidence indicates that endostatin inhibits fibrosis. However, the mechanism is yet to be clarified. The aim of this study is to evaluate the effect of endostatin on platelet-derived growth factor-BB （PDGF-BB）- or transforming growth factor β1 （TGF-β1）-induced fibrosis in cultured human skin fibroblasts, and to further examine the molecular mechanisms involved. Human dermal flbroblasts were cultured in Dulbecco＇s modified Eagle＇s medium （DMEM） and serum-starved for 48 h before treatment. Cells were grouped as follows： ＂PDGF-BB＂, ＂PDGF-BB＋ endostatin＂, ＂TGF-β1＂, ＂TGF-β1＋endostatin＂, ＂endostatin＂, and ＂blank control＂. The fibroblasts were stimulated with either TGF-β1 or PDGF-BB for 72 h in order to set up the fibrosis model in vitro. The cells were co-cultured with either TGF-β1 or PDGF-BB and endostatin and were used to check the inhibiting effect of endostatin. A blank control group and an endostatin group were used as negative control groups. The biomarkers of fibrosis, including the expression of collagen I, hydrroxyproline, and α-smooth muscle actin （a-SMA）, were evaluated using an enzyme-linked immune- sorbent assay （ELISA） and Western blot. The expression of phosphorylated PDGF receptor β （p-PDGFRβ）, PDGFRβ, phosphorylated extracellular signal-regulated kinase （p-ERK）, and ERK was detected using Western blot and im- munofiuorescent staining was used to explore the mechanisms. Both PDGF-BB and TGF-β1 significantly up-regulated the expression of collagen I, hydroxyproline, and a-SMA. Endostatin significantly attenuated both the PDGF-BB- and TGF-β1-induced over-expression of collagen I, hydroxyproline, and a-SMA. PDGF-BB and TGF-β1 both promoted the expression of PDGFR, ERK, and p-ERK. Endostatin inhibited the expression of PDGFR and p-ERK but did not affect the expression of total ERK. Endostatin inhibited hypertrophic scar by modulating the PDGFRI3/ERK pathway. En- dostatin could be a promising multi-target drug in future fibrosis therapy.