Latest ArticlesA UPCC-Q-TOF-MS method was established to analyze the components of polyoxyethylene 35 castor oil. The separation was performed at 50℃ on a Waters Acquity UPCC system by an Torus Diol column (3.0 mm×100 mm, 1.7 μm) with gradient elution of CO2 and methanol-acetonitrile (50:50); the flow rate was 1.0 mL·min-1, the back pressure was 2 000 psi, and methanol containing 2.5 mmol·L-1 ammonium formate was used as ionization reagent, whose flow rate was 0.2 mL·min-1. Positive ion electrospray ionization (ESI) mode and MSE technology were used. The qualitative analyses were carried out by using precise mass information of the parent and product ions and a PCA model was established by UPCC-Q-TOF-MS. L-02 cells and RBL-2H3 cells were used to study the cytotoxicity and histamine release of CrEL samples in vitro. A total of 13 kinds of CrEL components were obtained and their structures were identified by UPCC-Q-TOF-MS, with 255 compounds in total. The percentage content of 13 types of components was calculated by the normalization method. The content of polyoxyethylene glycerol tri-ricinoleate (PGTri-ricinoleate) in all samples was 0.36%-2.80% and the main components were polyethylene glycol, polyethylene glycerol and polyoxyethylene glycerol mono-ricinoleate. All samples have different degrees of cytotoxicity and histamine release, which is negatively correlated with the content of PGTri-ricinoleate and positively correlated with the content of polyoxyethylene glycol fatty acid esters. The UPCC-Q-TOF-MS method is simple and rapid, has strong separation ability and high accuracy. It is suitable for the analysis of CrEL components. It is suggested that the fatty acid composition should be included in the monograph of CrEL for injection to increase the content of PGTri-ricinoleate and decrease the content of polyoxyethylene glycol fatty acid esters, so as to improve the product safety.
The aim of this study is to prepare acetaminophen sustained-release tablets by hot melt extrusion 3D printing technology based on the concept of "Quality by Design" (QbD). Firstly, the failure mode and effect analysis (FMEA) was used to determine the critical process parameters (CPPs), then full-factor experimental design was used to analyze the critical quality attributes (CQAs) and to establish the design space. The results showed that the content of plasticizer, the path spacing and the shell numbers are independent variable for the experimental design. The design space was concluded to be plasticizer content:9%, and the shell number:3-5, the path spacing:1.05-1.2 mm. In this study, 3D printing technology was used to prepare acetaminophen sustained-release tablets in accordance with the concept of QbD, which improved the durability of the process and ensured the uniform and controllable quality of the preparation and also provided experimental basis for personalised medicine.
Ischemic stroke is one of the leading causes of death and disability worldwide. A large number of preclinical studies have demonstrated that exogenous cell-based therapies such as mesenchymal stem cell transplantation can promote brain function recovery in the subacute phase of stroke. Emerging data indicate that mesenchymal stem cell-derived exosomes play a key role in mediating tissue repair by participating in intercellular signal transduction and transferring biological information especially microRNA to recipient cells, which affects endo-genous recovery in ischemic brain tissue after injury. In this review we briefly describe the characteristics and biological functions of exosomes and exosomal microRNA, and discuss the therapeutic effects of mesenchymal stem cell-derived exosomes on ischemic stroke from different perspectives. Finally, we outline the potential clinical value of exosomes and challenges of translating these therapies into clinical trials.
The tumor contains abundant new vessels, which are unevenly distributed, irregular, and branch-disordered. Angiopoietin (Ang) and tyrosine kinase receptor Tie mediate stable maturation of angiogenesis. Ang1 mainly plays a role in promoting vascular stabilization, and Ang2 is highly expressed in vessels, which makes the structure and function of vessels abnormal. Leaked vessels provide opportunities for invasion and metastasis of circulating tumor cells. Targeting the Ang/Tie axis to correct the abnormal state of vessels and promote its normalization, combined with chemotherapy drugs or immunotherapy, play a synergistic effect against tumors. This article summarizes the role of Ang/Tie axis in tumor angiogenesis and metastasis, and it aims to provide new ideas and strategies for clinical treatment of tumors.
We investigated the ability of 3-bromopyruvic acid to increase the sensitivity of tamoxifen-resistant MCF-7/TR cells to tamoxifen and to explore the underlying mechanism. 4-Hydroxy tamoxifen (4-OHT) is the active form of tamoxifen in vivo and was used in this study. The effect of 3-bromopyruvic acid on the viability of MCF-7/TR cells was measured by MTT assay and the morphology of MCF-7/TR cells was observed with an inverted microscope. The results show that 3-bromopyruvic acid at 40 μmol·L-1 has no significant effect on the viability of MCF-7/TR cells, and this concentration was used in the subsequent experiments:3-bromopyruvic acid significantly increased the inhibitory effect of 4-OHT on the viability of MCF-7/TR cells, with a reversal-fold of 1.91, as determined by MTT assay; the lactate level, determined with a lactate detection kit, and the expression levels of GLUT1, HK2, and LDHA in MCF-7/TR cells as measured by immunoblotting were significantly higher than in MCF-7 cells; and compared with 4-OHT treatment alone, the combination treatment of 3-bromopyruvic acid and 4-OHT significantly reduced the lactate level and the expression of GLUT1, HK2, LDHA in MCF-7/TR cells. The above results show that 3-bromopyruvic acid increases the sensitivity of MCF-7/TR cells to tamoxifen, and the mechanism is related to the inhibition of aerobic glycolysis.
In recent years, the number of clinical trials of stem cell products has increased, and the research and development technology and evaluation system have developed rapidly. Human pluripotent stem cell (hPSC)-derived cellular products are in the phase Ⅰ/Ⅱ stage of clinical trials. Related products include hPSC-derived neurons, retinal pigment epithelial cells, pancreatic beta cells, etc. They are generally used for the repair and replacement of functional cells related to degenerative diseases and genetic diseases via local transplantation. So far, no similar products have been officially approved on market. As hPSC possesses multi-directional differentiation potential and the ability to form teratoma in vivo, compared with other stem cell products, hPSC-derived cellular products have relatively higher risk of tumorigenicity, longer differentiation induction cycle, more complex production process, together with the rapidly updating quality characterization methods, which pose challenges to the scientific evaluation of their human applications. Based on the problems in the recent review and communication of clinical trial applications of stem cell products, and with reference to the relevant technical guidelines, this paper proposes the chemistry, manufacturing, and controls review considerations on the manufacturing process and quality study of hPSC-derived cellular products. We hope to improve the communications between developers and regulators.
The intestinal flora is a diverse microbial community living in the digestive tract of humans and animals. This microbial community can modify drugs in unpredictable ways, leading to changes in the pharmacokinetics of drugs in vivo and affecting their clinical efficacy. Here we review drug metabolism mediated by intestinal flora from three aspects:prodrug activation, drug inactivation, and toxicity. The effect of the stable hypoxic environment on the composition and quantity of intestinal flora and the effect on drug metabolism are discussed. Understanding the influence of intestinal flora on drug metabolism is not only conducive to individualized medication, but also conducive to rational drug design, allowing us to predict and understand individual drug response and regulate the intestinal microbiome to improve drug efficacy, thus promoting personalized medicine.
In recent years, with rapid advances in chlorogenic acid (CGA) research, it has become widely used in medicine, the chemical industry and health care products, with the potential for broad application. CGA is a water-soluble phenolic natural product and is extensively distributed in a variety of plants. Numerous studies have shown that CGA has strong biological activities including antibacterial, antiviral, antitumor, antioxidative, anti-inflammatory and metabolic regulatory activities. This review summarizes the pharmacological effects as well as the underlying mechanisms of CGA, providing an important theoretical basis for further research on CGA drug targets and potential mechanisms.
Malignant tumor is a disease that severely threaten human health. Common chemotherapeutical drugs currently used in clinical practice have some problems in severe side effects and chemoresistance. In contrast, natural venom peptides and artificially designed targeting peptides have excellent biological activities and potential druggability due to their small molecular weights and high affinity to tumor tissues. Thus, the methods for the discovery of anti-tumor peptides have attracted much attention. In this paper, we summarized the types of anti-tumor peptides from recent literatures. Then, we systematically reviewed screening theories, methods and applications based on traditional chromatographic separation, peptidomics, phage display, phenotypic screening, and artificial intelligence. These strategies and technologies will provide a methodological reference for accelerating anti-tumor peptides research.
Parkinson's disease (PD) is the second most common neurodegenerative disease of the central nervous system. It is currently believed that PD is related to factors such as age, gender, family inheritance, gene mutation and environment. The pathogenesis of PD is complex and is related to dysfunction and loss of dopaminergic neurons, involving accumulation of α-synuclein, neuroinflammation, oxidative stress, mitochondrial dysfunction and excessive accumulation of neuromelanin. In many ways, various factors act both independently and through cross-promotion, resulting in an ongoing pattern of brain tissue damage and progressing PD pathology. This article reviews the recent research on the pathogenic factors and pathogenesis of PD and explores new ideas and potential targets for PD treatment and drug development.
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