多组学联用在中药作用机制研究中的应用

组学技术的运用主要基于高通量分析检测技术,包括转录组学、蛋白质组学和代谢组学等。生物信息学的飞速发展,为探索中药治疗疾病的机制提供新的思路和方法。在过去的数十年间,组学技术广泛应用于中药作用机制的研究当中。中药具有多成分、多靶点的特点,单一通路研究难以诠释中药"整体观念"的治疗思想,而多组学联用研究与这一观点不谋而合。查阅近年文献,对转录组学、蛋白质组学、代谢组学及16S rRNA测序等联用在中药治疗疾病中发挥的作用进行综述。     

Microstructure and Interfacial Reactions of Resistance Brazed Lap Joints between TC4 Titanium Alloy and 304 Stainless Steel Using Metal Powder Interlayers

In the brazing joint between titanium alloy and stainless steel, a lot of Fe-Ti intermetallic compounds (IMCs) can be easily formed to make joints crack. A lap resistance brazing process with metal powder layers on both sides of the filler metal was used to solve this problem. The microstructure and metallurgical behavior of joints was studied through comparative experiments. The result showed that Nb, V and Cr powders and the solder reacted with the base material to form a new phase, which replaced the Ti-Fe brittle phase in the joint. At the same time, metal powder clusters hindered the diffusion of Ti and Fe elements and improved the distribution of new phases. The established atomic reaction model revealed the metallurgical behavior and formation mechanism of the joints. Therefore, the intervening position of the metal powder layer and the multi-reaction zone structure are the main reasons the shear strength of joints is improved.     

虎杖苷药理作用及机制研究进展

虎杖苷是从传统中药虎杖中分离出的一种多酚类单体化合物，是虎杖的主要有效成分，具有多种药理活性。近年来，有关虎杖苷药理作用及机制的研究日益增多。现代药理学研究表明，虎杖苷对神经系统，心脑血管系统，呼吸系统等均有保护作用，对肝、肾、肺等器官亦作用明显，其调节血糖血脂的作用对抗动脉粥样硬化效果显著；其抗纤维化的作用对肝、肾保护效果明显。虎杖苷对多种肿瘤细胞均有抑制作用，可抑制肿瘤细胞增殖并诱导肿瘤细胞凋亡。虎杖苷还具有抗炎，保护骨髓，促进创面愈合，抗辐射等药理活性。笔者查阅有关虎杖苷的药理作用文献发现其单个药理作用机制往往受多靶点蛋白、多条通路调控，但大多还未明确其作用靶点，有待深入研究。该文就近5年来有关虎杖苷的药理作用及机制研究进展进行归纳总结，并对其研究现状及未来研究方向提出相关建议，以期拓宽科研者的研究思路，加快明确其发挥药效作用的靶点，为虎杖苷的进一步开发利用提供科学的理论依据。     

慢性疼痛中枢调控网络的研究现状与思考＊

慢性疼痛是一种复杂的身心疾病，包括躯体痛觉异常、认知障碍、负性情绪等多个方面的改变，同时伴随着神经系统的功能以及结构的改变。本文将对慢性疼痛与下行疼痛调节通路、疼痛情感-认知调控网络以及中脑边缘奖赏网络的相关性，以及针刺镇痛的中枢机制相关研究文献进行综述，旨在探讨下行疼痛调节通路、疼痛情感-认知调控网络以及中脑边缘奖赏网络在慢痛发生机制中的作用，为临床治疗慢性疼痛类疾病提供更优势的治疗方案。     

基于网络药理学和实验验证探讨路氏润燥汤治疗干燥综合征的分子机制＊

目的 通过网络药理学探索路氏润燥汤治疗干燥综合征的可能作用机制，并通过动物实验进行验证。方法 通过TCMSP数据库检索收集路氏润燥汤方中各药物生物信息，通过Genecard数据库检索收集干燥综合征的靶标蛋白，将药物和疾病的靶点信息进行交集，获得交集信息。将信息导入STRING平台获得PPI网络图，将筛选的得到的药物成分与靶点信息通过Cytospace软件构建“成分-靶点”网络图，利用DAVID数据库进行GO富集分析和KEGG通路分析。通过动物实验对网络药理学预测出的通路信息进行验证。结果 路氏润燥汤主要通过影响肿瘤坏死因子、细胞因子，肿瘤坏死因子信号通路、IL-17信号通路等信号通路来治疗干燥综合征。结论 路氏润燥汤是通过多靶点、多通路来治疗干燥综合征，网络药理学可以对路氏润燥汤进行较为全面的预测，有助于临床实验研究。     

DNA损伤在衰老相关疾病中的研究进展

DNA损伤是衰老相关疾病领域的研究热点, 可引起细胞周期停滞、凋亡, 加快个体衰老速度、增加衰老相关疾病的患病风险。本文将从细胞衰老和个体衰老两个层面阐述其与衰老之间的研究进展, 并综述其与衰老常见相关疾病(肿瘤、心血管疾病、阿尔茨海默病)及早衰综合征的关系, 为抗衰老研究和临床干预衰老相关疾病提供理论依据。     

罗布麻的抗衰老作用机制研究

目的 探讨罗布麻的抗衰老作用机制。方法 利用网络药理学预测罗布麻抗衰老相关的活性成分、作用靶点、分子功能、信号通路；利用衰老小鼠模型对罗布麻的抗衰老作用及其关键靶点进行验证。结果 网络药理学预测得到罗布麻抗衰老相关的9个活性成分、85个关键靶点、116个分子功能和163条信号通路；动物模型验证了罗布麻减轻D-半乳糖导致的小鼠衰老表型，下调P53的表达。结论 罗布麻含有多种活性成分，通过调控P53等靶点，发挥其衰老作用。     

Small nucleolar RNA host gene 3 functions as a novel biomarker in liver cancer and other tumour progression

Cancer has become the most life-threatening disease in the world. Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs, especially long noncoding RNAs (lncRNAs), have significant effects in human cancers. LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes. Small nucleolar RNA host gene 3 (SNHG3) is a novel lncRNA and has been reported to be differentially expressed in various tumors, such as liver cancer, gastric cancer, and glioma. However, the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood. In this review, we summarize the results of SNHG3 studies in humans, animal models, and cells to underline the expression and role of SNHG3 in cancer. SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis. SNHG3 expression in lung adenocarcinoma remains controversial. Concurrently, SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms, including competing endogenous RNA effects. A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.     

Melatonin and its metabolites as copper chelating agents and their role in inhibiting oxidative stress: a physicochemical analysis

The copper sequestering ability of melatonin and its metabolites cyclic 3‐hydroxymelatonin (3OHM), N¹‐acetyl‐N²‐formyl‐5‐methoxykynuramine (AFMK), and N¹‐acetyl‐5‐methoxykynuramine (AMK) was investigated within the frame of the Density Functional Theory. It was demonstrated that these compounds are capable of chelating copper ions, yielding stable complexes. The most likely chelation sites were identified. Two different mechanisms were modeled, the direct‐chelation mechanism (DCM) and the coupled‐deprotonation‐chelation mechanism (CDCM). It is proposed that, under physiological conditions, CDCM would be the main chelation route for Cu(II). It was found that melatonin and its metabolites fully inhibited the oxidative stress induced by Cu(II)‐ascorbate mixtures, via Cu(II) chelation. In the same way, melatonin, AFMK, and 3OHM also prevented the first step of the Haber–Weiss reaction, consequently turning off the ˙OH production via the Fenton reaction. Therefore, it is proposed that, in addition to the previously reported free radical scavenging cascade, melatonin is also involved in a concurrent ‘chelating cascade’, thereby contributing to a reduction in oxidative stress. 3OHM was identified as the most efficient of the studied compounds for that purpose, supporting the important role of this metabolite in the beneficial effects of melatonin against oxidative stress.