作者机构：
[Wang, Weiguo; Yang, ZeHua; Yang, Lin; He, Jian; Cao, Qianqian; Zhang, Ruilin] Univ South China, Inst Pharm & Pharmacol, Hengyang 421000, Hunan, Peoples R China.;[Wang, Weiguo; Yang, ZeHua; Yang, Lin; He, Jian; Cao, Qianqian; Zhang, Ruilin] Hunan Xinhexin Biol Med Co Ltd, Pharm Grad Educ Innovat Base, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Hengyang 421000, Hunan, Peoples R China.;[Wang, Qiao] Univ South China, Affiliated Hosp 1, Dept Ultrasound Imaging, Hengyang Med Coll, Hengyang 421001, Hunan, Peoples R China.;[Chen, Zhixi] Univ South China, Affiliated Hosp 1, Hengyang Med Coll, Blood Transfus Dept, Hengyang 421001, Hunan, Peoples R China.;[Chen, Weiwei] Univ South China, Hengyang Med Coll, Hengyang 421000, Hunan, Peoples R China.
通讯机构：
[Weiguo Wang] I;Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421000, Hunan, China<&wdkj&>Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang 421000, Hunan, China<&wdkj&>Hunan Xinhexin Biological Medicine Co., Ltd., Pharmacy Graduate Education Innovation Base, Hengyang 421000, Hunan, China
作者机构：
[Fu, Yuting; Jiang, Binyuan; Yuan, Yeqin] Univ South China, Affiliated Changsha Cent Hosp, Med Res Ctr, Hengyang Med Sch, Changsha 410004, Peoples R China.;[Zhou, Ziwei; Long, Huizhi] Univ South China, Sch Pharm, Hengyang Med Sch, Hengyang 421001, Peoples R China.;[Jiang, Binyuan] Univ South China, Affiliated Changsha Cent Hosp, Hengyang Med Sch, Dept Clin Lab, Changsha 410004, Peoples R China.
通讯机构：
[Binyuan Jiang] M;Medical Research Center, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha 410004, China<&wdkj&>Department of Clinical Laboratory, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha 410004, China<&wdkj&>Author to whom correspondence should be addressed.
关键词：
breast cancer;clinical trial drugs;natural products;PI3K–AKT pathway
摘要：
Glioblastoma multiform (GBM), one of the most common, aggressive primary brain tumours, demonstrates resistance to radiotherapy and chemotherapy after surgical resection and treatment failure. Metformin (MET) has been shown to suppress the proliferative capacity and invasion ability of GBM cells by activating AMPK and inhibiting mTOR, but the effective dose exceeded the maximum tolerated dose. Artesunate (ART) can exert certain anti-tumour effects by activating the AMPK-mTOR axis and inducing autophagy in tumour cells. Therefore, this study investigated the effects of MET combined with ART combination therapy on autophagy and apoptosis in GBM cells. MET combined with ART treatment effectively suppressed the viability, mono-cloning ability, migration and invasion capacities, as well as metastatic ability of GBM cells. The underlying mechanism involved modulation of the ROS-AMPK-mTOR axis, which was confirmed using 3-methyladenine and rapamycin to inhibit or promote the effects of MET combined with ART, respectively. The study findings suggest that MET used in combination with ART can induce autophagy-dependent apoptosis in GBM cells by activating the ROS-AMPK-mTOR pathway, providing a potential new treatment for GBM.
作者机构：
[Yang, Qinglai; He, Yuxuan] Univ South China, Hengyang Med Sch, Dept Biochem & Mol Biol, Hengyang 421001, Peoples R China.;[Tang, Li; Yang, Qinglai; Li, Na; Tan, Xiaofeng; He, Yuxuan; Yang, Sha] Univ South China, Canc Res Inst, Hunan Prov Key Lab Tumor Cellular & Mol Pathol, Hengyang Med Sch,Ctr Mol Imaging Probe, Hengyang 421001, Peoples R China.;[Tang, Li] Hainan Normal Univ, Coll Chem & Chem Engn, Key Lab Trop Med Plant Chem, Minist Educ, Haikou 571158, Peoples R China.
通讯机构：
[Qinglai Yang] D;Department of Biochemistry and Molecular Biology, Hengyang Medica School, University of South China, Hengyang 421001, China<&wdkj&>Center for Molecular Imaging Probe, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang 421001, China<&wdkj&>Author to whom correspondence should be addressed.
摘要：
In recent years, pathogenic infections have been a growing health threat due to the proliferation of drug-resistant bacteria, so photothermal therapy (PTT) has gained considerable interest in biological and medical fields, owing to its noninvasive and highly effective properties. However, it is hard to achieve selective bacteria targeting while generating a large amount of heat at infected sites. Cationic electrostatic interaction is considered to be a common antimicrobial strategy. Herein, an organic molecule named RT-MN was synthesized with four positively charged quaternary ammonium salts that can bind to negatively charged bacteria. Under near-infrared 808 nm laser irradiation, RT-MN could be efficiently converted into a large amount of heat to eradicate bacteria. In addition, its good water solubility and biological safety proved that RT-MN has excellent biological application prospects. Overall, four such positively charged photosensitizer RT-MN, as a non-antibiotic treatment for resistant bacteria, could be promising for the exploration of highly effective antibacterial agents.
摘要：
With the development of the social economy, unhealthy living habits and eating styles are gradually affecting people's health in recent years. As a chronic liver disease, NAFLD is deeply affected by unhealthy living habits and eating styles and has gradually become an increasingly serious public health problem. As a protein complex in clinical research, the inflammasomes play a crucial role in the development of NAFLD, atherosclerosis, and other diseases. This paper reviews the types, composition, characteristics of inflammasomes, and molecular mechanism of the inflammasome in NAFLD. Meanwhile, the paper reviews the drugs and non-drugs that target NLRP3 inflammasome in the treatment of NAFLD in the past decades. we also analyzed and summarized the related experimental models, mechanisms, and results of NAFLD. Although current therapeutic strategies for NAFLD are not effective, we expect that we will be able to find an appropriate treatment to address this problem in the future with further research on inflammasome.
作者：
Ren, Jieyu;Zeng, Qun;Wu, Hongmei;Liu, Xuewen;Guida, Maria C.;...
期刊：
JOURNAL OF CELLULAR PHYSIOLOGY,2023年238(3):647-658 ISSN：0021-9541
通讯作者：
Min Tang<&wdkj&>Min Tang Min Tang Min Tang
作者机构：
[Zeng, Qun; Li, Junjie; Wu, Hongmei; Liu, Xuewen; Tang, Min; Ren, Jieyu; Zhai, Yiyuan] Univ South China, Coll Hengyang Med, Dept Biochem & Mol Biol, Hengyang, Peoples R China.;[Ocorr, Karen; Guida, Maria C.; Bodmer, Rolf] Sanford Burnham Prebys Med Discovery Inst, Dev Aging & Regenerat Program, La Jolla, CA USA.;[Huang, Wen] Cent South Univ, Ctr Med Genet, Sch Life Sci, Changsha, Hunan, Peoples R China.;[Tang, Min] Univ South China, Changsheng West Rd 28,, Hengyang 421001, Peoples R China.
通讯机构：
[Min Tang; Min Tang Min Tang Min Tang] D;Department of Biochemistry and Molecular Biology, College of Hengyang Medical, University of South China, Hengyang, China
摘要：
Cardiomyopathy is a common disease of cardiac muscle that negatively affects cardiac function. HDAC3 commonly functions as corepressor by removing acetyl moieties from histone tails. However, a deacetylase-independent role of HDAC3 has also been described. Cardiac deletion of HDAC3 causes reduced cardiac contractility accompanied by lipid accumulation, but the molecular function of HDAC3 in cardiomyopathy remains unknown. We have used powerful genetic tools in Drosophila to investigate the enzymatic and nonenzymatic roles of HDAC3 in cardiomyopathy. Using the Drosophila heart model, we showed that cardiac-specific HDAC3 knockdown (KD) leads to prolonged systoles and reduced cardiac contractility. Immunohistochemistry revealed structural abnormalities characterized by myofiber disruption in HDAC3 KD hearts. Cardiac-specific HDAC3 KD showed increased levels of whole-body triglycerides and increased fibrosis. The introduction of deacetylase-dead HDAC3 mutant in HDAC3 KD background showed comparable results with wild-type HDAC3 in aspects of contractility and Pericardin deposition. However, deacetylase-dead HDAC3 mutants failed to improve triglyceride accumulation. Our data indicate that HDAC3 plays a deacetylase-independent role in maintaining cardiac contractility and preventing Pericardin deposition as well as a deacetylase-dependent role to maintain triglyceride homeostasis.
通讯机构：
[Mi, PB; Yao, X; Zheng, X ] U;Univ South China, Inst Pharm & Pharmacol, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;Hunan Vocat Coll Sci & Technol, Dept Pharm, Third Zhongyi Shan Rd, Changsha 410004, Hunan, Peoples R China.
关键词：
Ursolic acid derivatives;Structure–activity relationship;Anti-lung cancer activities;IC50;Mechanism
摘要：
As one of the most common mortal diseases, the development of anti-lung cancer drugs is never stopped. Ursolic acid (UA) is a pentacyclic triterpenoid with significant anti-lung cancer activity and low toxicity. The bottleneck of UA in clinical application is poor water solubility and bioavailability. Until now, many novel UA derivatives have been developed to overtake these problems. In this paper, the relationship between the structure and activity of different functional groups was discussed. All anti-lung cancer ursolic acid derivatives were reviewed, and their biological activity and structure-activity relationship were described. The research progress of UA derivatives against various types of lung cancer was reviewed.
摘要：
A core transcription regulatory circuitry (CRC) is an interconnected self-regulatory circuitry that is formed by a group of core transcription factors (TFs). These core TFs collectively regulate gene expression by binding not only to their own super enhancers (SEs) but also to the SEs of one another. For most human tissue/cell types, a global view of CRCs and core TFs has not been generated. Here, we identified numerous CRCs using two identification methods and detailed the landscape of the CRCs driven by SEs in large cell/tissue samples. The comprehensive biological analyses, including sequence conservation, CRC activity and genome binding affinity were conducted for common TFs, moderate TFs, and specific TFs, which exhibit different biological features. The local module located from the common CRC network highlighted the essential functions and prognostic performance. The tissue-specific CRC network was highly related to cell identity. Core TFs in tissue-specific CRC networks exhibited disease markers, andhad regulatory potential for cancer immunotherapy. Moreover, a user-friendly resource named CRCdb (http://www.licpathway.net/crcdb/index.html) was developed, which contained the detailed information of CRCs and core TFs used in this study, as well as other interesting results, such as the most representative CRC, frequency of TFs, and indegree/outdegree of TFs.
摘要：
Long non-coding RNAs are RNA molecules with a transcript length of more than 200 nucleotides and without protein-coding ability. They regulate gene expression by interacting with protein, RNA and DNA. Their function is closely related to their subcellular localization, with regulation of gene expression at the epigenetic and transcriptional levels occurring in the nucleus, and at the post-transcriptional and translational levels in the cytoplasm. Long stress-induced non-coding transcript 5 (LSINCT5), which is localized in the nucleus, is overexpressed in many types of cancers such as breast cancer, gastric cancer, ovarian cancer, thyroid cancer, and gastrointestinal cancer. Substantial evidence indicates that there is an obvious connection between cancers and LSINCT5, as it inhibits apoptosis and promotes proliferation, invasion and migration of cancer cells, as well as participates in the pathogenesis and progression of cancer by interacting with DNA, protein and RNA. These findings suggest that LSINCT5 could be a novel biomarker and an emerging therapeutic target in human cancers. In the present study, the structure and corresponding biological function of LSINCT5 were summarized in order to clarify its molecular mechanisms in the progression of various malignant tumors.
摘要：
This study aimed to investigate the effect of miRNAs involving oxidative stress response in doxorubicin (DOX)-induced cardiotoxicity based on the data from Gene Expression Omnibus (GEO) database and experimental results via integrated bioinformatics analysis. MiRNA expression profiles of DOX-induced cardiotoxicity in rat myocardial tissues and adult rat cardiomyocytes (ARC) were extracted from GEO datasets (GSE36239). Differential expression miRNA (DEMs) were separately captured in rat myocardial tissues and in ARC, and intersected between rat myocardial tissues and ARC via Venny 2.1. Subsequently, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) analyzed 46 target genes of miR-143, one of 6 DEMs, and HIF-1 and PI3K-Akt signaling pathway were significantly enriched. Further experimental results showed DOX-induced oxidative stress downregulated the expression of miR-143, and then promoted target gene Bbc3 expression and H9c2 apoptosis, the intervention of phosphocreatine (PCr) or N-acetyl-L-cystine (NAC) alleviated oxidative stress, apoptosis and Bbc3 expression, upregulated miR-143 in DOX-induced cardiotoxicity in vivo and in vitro. Our findings elucidated the regulatory network between miR-143 and oxidative stress in DOX-induced cardiotoxicity, and might unveiled a potential biomarker and molecular mechanisms, which could be helpful to the diagnosis and treatment of DOX-induced cardiotoxicity.
通讯机构：
[Hai-Tao Wu; Ling-Ling Zhu] D;[Li-Ying Wu] S;Department of Neurobiology, Beijing Institute of Basic Medical Sciences , Beijing , People’s Republic of China<&wdkj&>Department of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University , Nantong , People’s Republic of China<&wdkj&>Department of Pharmacology, University of Nanhua , Hengyang , China<&wdkj&>State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine , Beijing , People’s Republic of China<&wdkj&>Department of Neurobiology, Beijing Institute of Basic Medical Sciences , Beijing , People’s Republic of China<&wdkj&>Department of Neurobiology, Beijing Institute of Basic Medical Sciences , Beijing , People’s Republic of China
摘要：
Hypoxia as a microenvironment or niche stimulates proliferation of neural stem cells (NSCs). However, the underlying mechanisms remain elusive. Autophagy is a protective mechanism by which recycled cellular components and energy are rapidly supplied to the cell under stress. Whether autophagy mediates the proliferation of NSCs under hypoxia and how hypoxia induces autophagy remain unclear. Here, we report that hypoxia facilitates embryonic NSC proliferation through HIF-1/mTORC1 signaling pathway-mediated autophagy. Initially, we found that hypoxia greatly induced autophagy in NSCs, while inhibition of autophagy severely impeded the proliferation of NSCs in hypoxia conditions. Next, we demonstrated that the hypoxia core regulator HIF-1 was necessary and sufficient for autophagy induction in NSCs. Considering that mTORC1 is a key switch that suppresses autophagy, we subsequently analyzed the effect of HIF-1 on mTORC1 activity. Our results showed that the mTORC1 activity was negatively regulated by HIF-1. Finally, we provided evidence that HIF-1 regulated mTORC1 activity via its downstream target gene BNIP3. The increased expression of BNIP3 under hypoxia enhanced autophagy activity and proliferation of NSCs, which was mediated by repressing the activity of mTORC1. We further illustrated that BNIP3 can interact with Rheb, a canonical activator of mTORC1. Thus, we suppose that the interaction of BNIP3 with Rheb reduces the regulation of Rheb toward mTORC1 activity, which relieves the suppression of mTORC1 on autophagy, thereby promoting the rapid proliferation of NSCs. Altogether, this study identified a new HIF-1/BNIP3-Rheb/mTORC1 signaling axis, which regulates the NSC proliferation under hypoxia through induction of autophagy.
通讯机构：
[Zifen Guo; Hua Wei; Cui-Yun Yu; Zifen Guo Zifen Guo Zifen Guo; Hua Wei Hua Wei Hua Wei; Cui-Yun Yu Cui-Yun Yu Cui-Yun Yu] H;Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pharmacy & Pharmacology, School of Pharmaceutical Science, Hengyang Medical School, University of South China, Hengyang, 421001 China
摘要：
This review summarizes four leading strategies used to promote the therapeutic effects of immunogenic cell death (ICD) via nanotechnology, including increasing the localized concentration of an ICD inducer in tumor, inducing various intracellular reactions, catalyzing the activity of antigen‐presenting cells, and protecting the function of cytotoxic T cells, together with an overview of the state‐of‐the‐art clinical applications of ICD via nanotechnology. Abstract Immunotherapy represents the most promising treatment strategy for cancer, but suffers from compromised therapeutic efficiency due to low immune activity of tumor cells and an immunosuppressive microenvironment, which significantly hampers the clinical translations of this treatment strategy. To promote immunotherapy with desired therapeutic efficiency, immunogenic cell death (ICD), a particular type of death capable of reshaping body's antitumor immune activity, has drawn considerable attention due to the potential to stimulate a potent immune response. Still, the potential of ICD effect remains unsatisfactory because of the intricate tumor microenvironment and multiple drawbacks of the used inducing agents. ICD has been thoroughly reviewed so far with a general classification of ICD as a kind of immunotherapy strategy and repeated discussion of the related mechanism. However, there are no published reviews, to the authors’ knowledge, providing a systematic summarization on the enhancement of ICD via nanotechnology. For this purpose, this review first discusses the four stages of ICD according to the development mechanisms, followed by a comprehensive description on the use of nanotechnology to enhance ICD in the corresponding four stages. The challenges of ICD inducers and possible solutions are finally summarized for future ICD‐based enhanced immunotherapy.
期刊：
CURRENT NEUROPHARMACOLOGY,2023年21(11):2251-2265 ISSN：1570-159X
通讯作者：
Tang, XQ
作者机构：
[Wang, Chun-Yan; Qiu, Zheng-Jie] Univ South China, Hengyang Med Coll,Key Lab Arteriosclerol Hunan Pr, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hunan Int Sci & Technol Cooperat Base Arterioscle, Hengyang 421001, Hunan, Peoples R China.;[Zhang, Ping] Univ South China, Hengyang Med Sch, Affiliated Nanhua Hosp, Dept Neurol, Hengyang 421001, Hunan, Peoples R China.;[Tang, Xiao-Qing] Univ South China, Hengyang Med Coll, Inst Neurosci, Hengyang Key Lab Neurodegenerat & Cognit Impairme, Hengyang 421001, Hunan, Peoples R China.;[Tang, XQ] Univ South China, Dept Physiol, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.;[Tang, XQ] Univ South China, Hengyang Med Sch, Inst Neurosci, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Tang, XQ ] U;Univ South China, Dept Physiol, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Hengyang Med Sch, Inst Neurosci, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.
关键词：
Central nervous system;DEC1;Neurodegenerative disease;Parkinson's disease;Pathogenesis;Transcription factor
摘要：
Differentiated embryo-chondrocyte expressed gene1 (DEC1), an important transcription factor with a basic helix-loop-helix domain, is ubiquitously expressed in both human embryonic and adult tissues. DEC1 is involved in neural differentiation and neural maturation in the central nervous system (CNS). Recent studies suggest that DEC1 protects against Parkinson's disease (PD) by regulating apoptosis, oxidative stress, lipid metabolism, immune system, and glucose metabolism disorders. In this review, we summarize the recent progress on the role of DEC1 in the pathogenesis of PD and provide new insights into the prevention and treatment of PD and neurodegenerative diseases.
关键词：
Anti-breast cancer activities;Baker-Venkataraman reaction;Fluorinated-genistein derivatives;Genistein;MTT assay;structure-activity relationship
摘要：
Background: Genistein has been limited in clinical application due to its low bioavailability, extremely poor liposolubility, and fast glycosylation rate, though it possesses anti-breast cancer activity. Therefore, the discovery of novel genistein derivatives is an urgency.<&wdkj&>Objective: To enhance the anti-breast cancer activity of genistein, a series of novel fluorinated genistein derivatives were synthesized.<&wdkj&>Methods: Their in vitro antitumor activity was investigated by the MTT assay against three cancer cell lines, via, MDA-MB-231, MCF-7, and MDA-MB-435, respectively.<&wdkj&>Results: Analogs 1d, 2b, and 3b showed remarkable anticancer activities compared to tamoxifen, a clinical anti-breast cancer drug on the market.<&wdkj&>Conclusion: The activities against breast cancer of genistein were enhanced by introducing the 7- alkoxyl group and fluorine atom into the B-ring. Therefore, these compounds may be potential candidates for treating breast cancer.
期刊：
Molecular and Cellular Biochemistry,2023年 ISSN：0300-8177
通讯作者：
Jiang, Zhisheng
作者机构：
[He, Shuya; He, Siqi; Jiang, Zhisheng; Ma, Yun; Gu, Tianhe] Univ South China, Inst Biochem & Mol Biol, Hengyang Med Coll, Hengyang 421001, Hunan, Peoples R China.;[Jiang, Zhisheng; Ma, Yun] Univ South China, Inst Cardiovasc Dis, Hengyang Med Sch, Key Lab Arteriosclerol Hunan Prov,Hunan Int Sci &, Hengyang 421001, Hunan, Peoples R China.;[Ma, Yun] Univ South China, Hengyang Med Sch, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Jiang, Zhisheng] I;Institute of Biochemistry and Molecular Biology, Hengyang Medical College, University of South China, Hengyang, 421001, Hunan, China.;Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hengyang Medical School, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, University of South China, Hengyang, 421001, Hunan, China.
摘要：
Cardiovascular disease (CVD) has a high incidence and low cure rate worldwide, and atherosclerosis (AS) is the main factor inducing cardiovascular disease, of which lipid deposition in the vessel wall is the main marker of AS. Currently, although statins can be used to lower lipids and low-density lipoprotein (LDL) in AS, the cure rate for AS remains low. Therefore, there is an urgent need to develop new therapeutic approaches, and stem cells are now widely studied, while stem cells are a class of cell types that always maintain the ability to differentiate and can differentiate to form other cells and tissues, and stem cell transplantation techniques have shown efficacy in the treatment of other diseases. With the establishment of cellular therapies and continued research in stem cell technology, stem cells are also being used to address the problem of AS. In this paper, we focus on recent research advances in stem cell therapy for AS and briefly summarize the relevant factors that induce the formation of AS. We mainly discuss the efficacy and application prospects of mesenchymal stem cells (MSCs) for the treatment of AS, in addition to the partial role and potential of exosomes in the treatment of AS. Further, provide new ideas for the clinical application of stem cells.
摘要：
HYPOTHESIS: Construction of dual gatekeepers-functionalized mesoporous organic silica nanoparticles (MONs) with both physical and chemical mechanisms for modulated drug delivery properties provides one solution to the extracellular stability vs. intracellular high therapeutic efficiency of MONs that hold great potential for clinical translations. EXPERIMENTS: We reported herein facile construction of diselenium-bridged MONs decorated with dual gatekeepers, i.e., azobenzene (Azo)/polydopamine (PDA) for both physical and chemical modulated drug delivery properties. Specifically, Azo can act as a physical barrier to block DOX in the mesoporous structure of MONs for extracellular safe encapsulation. The PDA outer corona serves not only as a chemical barrier with acidic pH-modulated permeability for double insurance of minimized DOX leakage in the extracellular blood circulation but also for inducing a PTT effect for synergistic PTT and chemotherapy of breast cancer. FINDINGS: An optimized formulation, DOX@(MONs-Azo3)@PDA resulted in approximately 1.5 and 2.4 fold lower IC50 values than DOX@(MONs-Azo3) and (MONs-Azo3)@PDA controls in MCF-7 cells, respectively, and further mediated complete tumor eradication in 4T1 tumor-bearing BALB/c mice with insignificant systematic toxicity due to the synergistic PTT and chemotherapy with enhanced therapeutic efficiency.
作者机构：
[Zhou, Jing; Yao, Xu; Xiang, Yi-Jun; Liu, Shun] Univ South China, Inst Pharm & Pharmacol, Hunan Prov Key Lab Tumor Microenvironm Respons Dru, Hengyang 421001, Peoples R China.;[Lin, Jin-Hong; Xiao, Ji-Chang; Xiang, Yi-Jun] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Organ Chem, Key Lab Organofluorine Chem, Shanghai 200032, Peoples R China.;[Lin, Jin-Hong] Shanghai Univ, Innovat Drug Res Ctr, Dept Chem, Shanghai 200444, Peoples R China.
通讯机构：
[Jin-Hong Lin; Ji-Chang Xiao] K;[Xu Yao] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, University of South China, 421001 Hengyang, PR China<&wdkj&>Key Laboratory of Organofluorine Chemistry, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, 200032 Shanghai, PR China<&wdkj&>Key Laboratory of Organofluorine Chemistry, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, 200032 Shanghai, PR China<&wdkj&>Department of Chemistry, Innovative Drug Research Center, Shanghai University, 200444 Shanghai, PR China
摘要：
Described here is the R3P/ICH2CH2I-promoted dehydroxylative sulfonylation of alcohols with a variety of sulfinates. In contrast to previous dehydroxylative sulfonylation methods, which are usually limited to active alcohols, such as benzyl, allyl, and propargyl alcohols, our protocol can be extended to both active and inactive alcohols (alkyl alcohols). Various sulfonyl groups can be incorporated, such as CF3SO2 and HCF2SO2, which are fluorinated groups of interest in pharmaceutical chemistry and the installation of which has received increasing attention. Notably, all reagents are cheap and widely available, and moderate to high yields were obtained within 15 min of reaction time.
摘要：
Circular RNA (circRNA) is a class of RNA with the 5' and 3' ends connected covalently to form a closed loop structure and characterized by high stability, conserved sequences and tissue specificity, which is caused by special reverse splicing methods. Currently, it has become a hot spot for research. With the discovery of its powerful regulatory functions and roles, the molecular mechanisms and future value of circRNA in participating in and regulating biological and pathological processes are becoming increasingly apparent. Among them is the increasing prevalence of cardiovascular diseases (CVDs). Many studies have elucidated that circRNA plays a crucial role in the development and progression of CVDs. Therefore, circRNA shows its advantages and brilliant expectations in the field of CVDs. In this review, we describe the biogenesis, bioinformatics detection and function of circRNA and discuss the role of circRNA and its effects on CVDs, including atherosclerosis, myocardial infarction, cardiac hypertrophy and heart failure, myocardial fibrosis, cardiac senescence, pulmonary hypertension, and diabetic cardiomyopathy by different mechanisms. That shows circRNA advantages and brilliant expectations in the field of CVDs.
