壮医针挑疗法对哮喘小鼠肺组织中胸腺基质淋巴细胞生成素、T盒转录因子和锌指蛋白3mRNA表达的影响

目的:观察壮医针挑疗法对哮喘小鼠肺组织中T盒转录因子(T-bet)和锌指蛋白3(GATA 3)mRNA表达以及胸腺基质淋巴细胞生成素(TSLP)的影响,探讨其治疗哮喘的机制。方法:成年雌性BALB/c小鼠30只,随机分为对照组、模型组、针挑组,每组10只。采用卵清蛋白致敏及激发制备哮喘小鼠模型。选取"大椎""肺俞""定喘""风门""肾俞"及"脾俞"等穴,每天针挑1次,共治疗7次。采用RT-PCR法检测肺组织T-bet及GATA 3mRNA表达水平;免疫荧光法检测TSLP表达;HE染色观察肺组织病理变化。结果:和对照组比较,模型组小鼠肺内TSLP、GATA 3mRNA相对表达量均显著升高(P0.01),而Tbet mRNA相对表达量降低(P0.05)。和模型组比较,针挑组小鼠肺内TSLP、GATA 3mRNA相对表达量显著降低(P0.01),而T-bet mRNA相对表达量升高(P0.05)。针挑组小鼠肺组织上皮增厚减轻,气管血管周围炎性反应细胞浸润较少。结论:降低肺组织TSLP含量和GATA 3mRNA表达,提高T-bet mRNA表达,可能是壮医针挑疗法治疗哮喘的机制之一。     

救脑宁注射液对谷氨酸、5-羟色胺诱发大鼠皮质神经细胞内游离钙超负荷的影响

目的：探讨救脑宁注射液对谷氨酸（Glu）、5-羟色胺（5-HT）诱发大鼠皮质神经细胞内游离钙（〔Ca2 〕i）超负荷的影响。方法：以Fura-2／AM为细胞内钙离子的荧光指示剂，用双波长荧光分光光度计测定了急性分离的新生大鼠神经细胞〔Ca2 〕i的变化，观察Glu、5－HT对〔Ca2 〕i的影响及救脑宁注射液的干预作用。结果：Glu和5－HT剂量依赖性引起〔Ca2＋〕i增加，导致细胞内钙超载；救脑宁注射液可显著降低细胞内钙的升高，保护神经细胞免受Glu和5－HT的损害。结论：救脑宁注射液对中风病的治疗作用与其对抗Glu、5－HT等毒性物质的作用，抑制受体依赖性钙通道的开放，减少外钙的流入，有效地防止钙超载等机制有关。     

17-甲氧基-7-羟基-苯并呋喃查尔酮对心肌细胞内游离钙浓度及L-型钙电流的影响

目的:研究17-甲氧基-7-羟基-苯并呋喃查尔酮(YLSC)对H2O2诱导的心肌细胞内钙超载的拮抗作用及对L型钙电流(ICa-L)的影响.方法:采用SD大鼠乳鼠进行心肌细胞培养,实验分为①正常对照组;②H2O2组:上机前加入终浓度为0.3 mmol·L-1的H2O2;③预先给予低、中、高不同终浓度YLSC药物处理组:分别给予100,200,400 μmol·L-1YLSC的无血清培养基,孵育24 h,上机前加入终浓度为0.3 mmol· L-1H202,以Fluo-3/AM荧光指示剂负载,应用激光共聚焦显微镜技术,分别于加入H202后15 min内检测细胞内[Ca2+]i的变化;分离昆明种小鼠单个心室肌细胞,全细胞膜片钳技术记录YLSC对ICa-L的影响.结果:①与正常对照组比较,H202诱导的模型组细胞内[Ca2+]i增加60.43％±7.75％,而高、中、低YLSC预处理组[Ca2+]i分别增加38.39％±13.87％,14.49％±2.94％,-28.1％ ±1.52％,与模型组比较显著降低(P＜0.01).②YLSC可使心室肌细胞ICa-L的电流-电压(Ⅰ-Ⅴ)关系曲线上移,能改变ICa-L的激活和失活特征,使ICa-L的激活曲线和稳态失活曲线左移.结论:YLSC对心肌细胞钙离子通道有较好的阻断作用,能显著减轻H2O2诱导的心肌细胞内[Ca2+];超载.     

Growth inhibition and induction of apoptosis in human oral squamous cell carcinoma Tca-8113 cell lines by Shikonin was partly through the inactivation of NF-kappaB pathway

Shikonin, a naphthoquinone pigment isolated from the Chinese herbal therapeutic, Zicao, has been shown to exhibit antioxidant and anticancer effects. In this study, its ability to induce apoptosis in cultured Tca-8113 oral cancer cells was studied. Treatment of the Tca-8113 cells with a variety of concentrations of Shikonin (10-40 microm) resulted in dose- and time-dependent sequences of events marked by apoptosis, as shown by the loss of cell viability, chromatin condensation, internucleosomal DNA fragmentation and sub-G1 phase accumulation. Furthermore, apoptosis in the Tca-8113 cells was accompanied by the activation of protease caspase-8, -9, -3 and low expression of Bcl-2 protein. Interestingly, inactivation of the NF-kappaB pathway was found in shikonin-induced apoptosis in Tca-8113 cells. These results raise the possibility that the anti-tumor effects of Shikonin in Tca-8113 cells are at least partly through the inactivation of the NF-kappaB pathway and subsequent activation of protease caspase family. Pharmacological inhibition of the NF-kappaB activity by Shikonin might be a powerful treatment option for OSCC in which activation of NF-kappaB plays a critical role in tumor growth and progression.     

Effects of Korean red ginseng extract on the prevention of atopic dermatitis and its mechanism on early lesions in a murine model

Ethnopharmacological relevance

Korean red ginseng (KRG) has been shown to possess various biological activities including anti-inflammatory properties.

Aim of the study

We aimed to investigate the effects and mechanism of KRG on the prevention of atopic dermatitis (AD) using a mouse model.

Materials and methods

The effect of KRG in trinitrochlorobenzene (TNCB)-treated NC/Nga mice was assessed by measuring ear thickness, transepidermal water loss (TEWL), total serum IgE, histologic changes of lesional skin, mRNA and protein expression of thymic stromal lymphopoietin (TSLP) and tumor necrosis factor (TNF)-α, immunohistochemistry for tissue interleukin (IL)-4, IL-17, and interferon (IFN)-γ.

Results

KRG significantly reduced ear thickness. Oral administration of KRG significantly prevented the increase in TEWL induced by TNCB. The serum IgE level was significantly lower in the KRG group. Histologically, lymphocyte infiltration was markedly decreased by KRG. CD1a positive (CD1a+) cells were diminished by KRG. Immunohistochemically, KRG significantly suppressed the protein expression of TSLP and TNF-α. The mRNA expression of TSLP in the lesions was significantly reduced by KRG. These results demonstrate that oral administration of KRG may inhibit the development of AD-like skin lesions in NC/Nga mice by modifying TSLP, DCs, and at least in part, the Th2 response.

Conclusion

KRG may be a potential therapeutic modality for the prevention of AD.