Table of Content

Volume 25 Issue 6
26 June 2020

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Hepatoprotective effects of Yinchenzhufu decoction on intrahepatic cholestasis liver injury in mice induced by ANIT via suppressing TLR4/NF-κB pathway

WANG Qian, SU Huizong, LI Yue, TAN Bo, YAN Dongming, JIN Jingyi, QIU Furong

2020, 25(6):  601-609.  doi:10.12092/j.issn.1009-2501.2020.06.001

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AIM: To investigate the hepatoprotective effects of Yinchenzhufu decoction (YCZFD) via TLR4/NF-κB pathway on the hepatic injury in alpha-naphthyisothiocyanate (ANIT)-induced intrahepatic cholestasis mice. METHODS: Male C57BL/6 mice were administered with YCZFD for consecutive 10 days, and intrahepatic cholestasis mice model was induced by orally given ANIT at dose of 75 g/kg on the seventh day. On the last day, the blood samples and liver samples were collected 2 hours after oral administration of YCZFD. The serum biochemical index, liver histopathology, the change of bile acid contents in mice liver, and the expression of relative proteins in TLR4/NF-κB pathway were determined. RESULTS: Compared with the model group, YCZFD treatment group significantly improved the hepatic necrosis and reduced the inflammatory cell infiltration. The plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bile acid (TBA), and total bilirubin (TBIL) levels were significantly decreased, and the free and conjugated bile acids were both reduced. The expression of TLR4, IL-1β, IL-6, TNF-α, and MCP-1 were significantly decreased. CONCLUSION: YCZFD presents hepatoprotective effects on the hepatic injury in ANIT-induced intrahepatic cholestasis mice, which may be related to inhibiting the TLR4/NF-κB pathway, reducing the intrahepatic bile acids, and suppressing the inflammatory reaction.

Protective effect of dexamethasone implant on nephrotoxicity of adriamycin in rats

ZHANG Cheng, FAN Manli, WANG Kun, QIN Zhiqiang, ZHOU Lanlan

2020, 25(6):  610-617.  doi:10.12092/j.issn.1009-2501.2020.06.002

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AIM: To study the establishment of adriamycin nephropathy rat model and the protective effects and mechanisms of dexamethasone implants (DEXI) through renal capsule implantation. METHODS: The adriamycin-induced nephropathy model was built by injecting Adriamycin (4 mg/kg) and Adriamycin (3.5 mg/kg) was injected again after week into tail-vein in SD rats. Renal capsule puncture was performed in model group. The excipient control group injected intra-renal capsule with drug-free excipient (1.4 mg/kg). The experimental group (2.8, 1.4, 0.7 mg/kg) was given by intrarenal capsule injection and positive drug group (0.1 mg/kg, qd × 8 w) was made by intragastric administration. The rat weight, kidney function and blood biochemical were observed and detected during the experiment. After the experiment, rat kidneys were stained with periodic acid-schiff to observe the morphological changes of mesangial and basement and sirius red to observe the renal tissue collagen fibers, expression of podocin and CD2AP were detected by immunohistochemistry. RESULTS: The blood protein content of adriamycin rats decreased, total blood cholesterol, uric acid, blood creatinine and urea nitrogen increased (P<0.05 or P<0.01), mesangium and fibers increased. The expression of Podocin protein in kidney tissue decreased and the expression of CD2AP protein increased (P<0.05 or P<0.01). DEXI increased the weight and blood protein levels of adriamycin rats, reduced blood lipids and blood uric acid levels (P<0.05 or P<0.01), improved renal function and tissue damage, and regulated the abnormal expression and distribution of Podocin and CD2AP proteins (P<0.05 or P<0.01). CONCLUSION: These results suggest that injecting adriamycin into the tail vein can establish a stable kidney disease model. DEXI renal capsule implantation can improve adriamycin nephropathy injury, and its mechanism may be related to restoration the expression and distribution of Podocin and CD2AP proteins on podocyte slit diaphragm.

Breviscapine induced the apoptosis of non-small cell lung cancer A549 cells

WEI Weitian, CHEN Sheng, WANG Liang, ZENG Jian

2020, 25(6):  618-624.  doi:10.12092/j.issn.1009-2501.2020.06.003

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AIM: To analyze the apoptosis promoting effect of breviscapine on NSCLC cells and the growth of transplanted tumor and investigate the mechanism. METHODS: The apoptosis, Caspase-3 activity, Bax and Bcl-2 expression of A549 cells treated with 25, 50 and 100 μmol/L breviscapine were detected. The subcutaneous transplanted tumor model was constructed with A549 cells. The mice were intraperitoneally injected with 10 mg/kg and 20 mg/kg breviscapine every day. The size and weight of the tumor were observed every week. On the 21st day, the mice were killed and the tumor was obtained. The expression of Bax and Bcl-2 was detected by Western blot. Bax/Bcl-2 ratio was analyzed. Caspase-3 expression was detected by immunohistochemistry and apoptosis in the tumor was detected by TUNEL staining. RESULTS: Breviscapine increased the apoptosis rate of A549 cells. The results of enzyme labeling showed that Caspase-3 activity increased significantly after breviscapine treatment compared with the control group. Western blot showed that breviscapine could significantly inhibit the expression of anti-apoptosis protein Bcl-2, increase the expression of pro-apoptosis protein Bax, and increase the ratio of Bax/Bcl-2. In vivo, on the 14th and 21st day, the tumor size of the treatment group was significantly smaller than that of the control group, while the weight of nude mice was not significantly reduced. Western blot showed that breviscapine could upregulate the expression of Bax and down regulate the expression of Bcl-2 in the transplanted tumor, while the expression of Caspase-3 was significantly increased. TUNEL staining showed that the proportion of apoptosis increased significantly compared with the control after breviscapine treatment. CONCLUSION: Breviscapine can induce the apoptosis of A549 cells in vitro and in vivo. The mechanism may be that breviscapine upregulates Bax expression and downregulates Bcl-2 expression, increases Bax/Bcl-2 ratio, activates Caspase-3, resulting in A549 cell apoptosis.

Minocycline inhibits inflammatory corpuscle mediated pyroptosis and improves cognitive ability in Alzheimer's disease mice

SHENG Yongjia, LI Wenyan, ZHU Diwei, WANG Jin, GU Yanling

2020, 25(6):  625-632.  doi:10.12092/j.issn.1009-2501.2020.06.004

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AIM: To study the mechanism of minocycline (Mino) in inhibiting inflammatory corpuscle NLRP3-mediated pyroptosis and improving cognitive ability in Alzheimer's disease. METHODS: Lipopolysaccharide (LPS) was used to induce PC12 to construct a model of neuronal pyroptosis. The cells were divided into control group, LPS group and LPS+Mino group. CCK-8 assay was used to detect cell viability, flow cytometry was used to detect apoptotic level, and Western blot was used to detect the levels of key proteins NLRP3, ASC, Caspase-1 and pro-Caspase-1 in NLRP3 corpuscles, as well as the levels of GSDMD and p30-GSDMD. Enzyme-linked immunosorbent assay was used to detect the expression of interleukin-1β, interleukin-18 and tumor necrosis factor-α in culture medium. APP-PS1 mice were randomly divided into control group and experimental group. The experimental group was given intragastric administration of minocycline 50 μg. The cognitive and memory abilities of mice were tested by Morris test before and 3 weeks after administration. The expressions of NLRP3, ASC, Caspase-1 and pro-Caspase-1 in hippocampal CA3 region were detected after execution, and the expressions of inflammatory factors such as IL-1β, IL-18 and TNF-α were detected. RESULTS: Minocycline could inhibit LPS-induced pyroptosis. Cell viability in LPS+Mino group was significantly higher than that in LPS group, and the apoptotic rate was significantly lower than that in LPS group (P<0.05). The expression of NLRP3, ASC and Caspase-1 in LPS+Mino group was lower than that in LPS group, while the expression of p30-GSDMD was lower than that in LPS group, and GSDMD was higher than that in LPS group. The levels of IL-1β, IL-18 and TNF-α in culture medium were lower than those in LPS group, with significant difference (P<0.05). In animal experiments, minocycline could significantly improve the cognitive ability of mice. In Morris experiment, the latency of mice was shortened, which had statistical significance compared with the control group (P<0.05). At the same time, the number of times of mice crossing the platform increased significantly compared with the control group (P<0.05). The expression of key proteins NLRP3, ASC and Caspase-1 in NLRP3 corpuscle of mice in experimental group was lower than that in control group, while the expression of pyroptosis executive protein p30-GSDMD was lower than that in control group, GSDMD was higher than that in control group, and the levels of inflammatory factors IL-1β, IL-18 and TNF-α were lower than that in control group (P<0.05). CONCLUSION: Minocycline can inhibit the activation of NLRP3 corpuscle and the occurrence of neuronal pyroptosis, and improve the cognitive ability of mice with Alzheimer's disease.

Ginsenoside Rg1 protects HL-7702 cells against oleic acid-induced injury via aldolase/AMPK/PINK1 signalling

HU Wenyan, LI Mei, LIU Huabao, RAO Chunyan, LI Hongting

2020, 25(6):  633-639.  doi:10.12092/j.issn.1009-2501.2020.06.005

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AIM: To study the protective effects of ginsenoside Rg1 on HL-7702 cells injury induce by oleic acid (OA), and investigate its role in aldolase/AMPK/PINK1 signalling. METHODS: HL-7702 cells were cultured in vitro and divided into five groups: control group (C), oleic acid group (OA), OA+ginsenoside (Rg1) group, OA+compound C (CC) group, and OA+CC+Rg1 group. The viability of HL-7702 cells was determined by CCK8 assay and Hoechst staining. The apoptosis and mitochondrial membrane potentials of HL-7702 cells were measured using flow cytometry. ATP content in HL-7702 cells was observed. Western blot was used to detect the expression levels of Cleaved caspase-3, PINK1, MFN2, Aldolase and p-AMPK in HL-7702 cells. RESULTS: Compared with C group, the viability of cells in OA group was significantly decreased (P<0.05), the apoptotic rate and Cleaved caspase-3 expression were greatly increased (P<0.05), ATP level, mitochondrial membrane potentials (TMRE) and PINK1 expression were significantly decreased (P<0.05). Compared with OA group, the viability of cells in OA+Rg1 group was significantly increased (P<0.05), the apoptotic rate and Cleaved caspase-3 expression were greatly decreased (P<0.05), ATP level, mitochondrial membrane potentials (TMRE) and PINK1 expression were significantly increased (P<0.05). Compared with OA+Rg1 group, the viability of cells and p-AMPK expression level in OA+CC+Rg1 group was significantly decreased (P<0.05). Reducing the expression of aldolase in cells inhibited Rg1?s actions on PINK1 and p-AMPK and cell viability. CONCLUSION: Ginsenoside Rg1 can improve the injury of HL-7702 cells via regulating aldolase/AMPK/PINK1 signaling pathway.

A novel model-assisted design in phase I clinical trials: Bayesian optimal interval design

ZHONG Zihang, CHEN Feng, YUAN Ying, CHENG Jiancheng, YU Xuanxuan, YANG Min, TAN Mingmin, ZHAO Yang, BAI Jianling, YU Hao

2020, 25(6):  640-648.  doi:10.12092/j.issn.1009-2501.2020.06.006

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AIM: To introduce a novel and flexible model-assisted design for Phase I clinical trials: Bayesian optimal interval (BOIN) design, including the process of implementation, practical implementation, and evaluation of its performance. METHODS: BOIN design decides dose escalation/de-escalation by comparing the observed toxicity rate at the current dose with an escalation boundary and a de-escalation boundary that are optimized to minimize the probability of making incorrect decision of dose assignment. The application of the BOIN design is illustrated using a trial example. RESULTS: BOIN combines the advantages of the algorithm-based methods and model-based methods. It enjoys desirable statistical properties -it is optimal, safe, robust and easy to implement. Simulation study shows that the BOIN substantially outperforms the existing designs with higher accuracy to identify the maximum tolerated dose (MTD). CONCLUSION: BOIN design possesses the similar statistical performance to the much more complicated model-based designs. It is simple to implement, and easy to calibrate to meet the safety requirement mandated by regulatory agents. The BOIN design has been widely used in different types of cancers. It is a novel design that holds great potential to substantially improve phase I trials in China.

Mechanism of saffron in treating atherosclerosis based on network pharmacology method

LI Mengying, SI Mingdong, WEN Zishuai, SHI Huan, LI Xinrui, ZHANG Yuanyuan, WANG Hongfang, MA Donglai, CHU Li

2020, 25(6):  649-657.  doi:10.12092/j.issn.1009-2501.2020.06.007

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AIM: To investigate the active components and potential mechanism of saffron (Crocus sativus L.) in inhibiting atherosclerotic lesion by using network pharmacological method. METHODS: TCMSP database was used to systematically analyze the active components of saffron. At the same time, GeneCards and OMIM databases were used to analyze the genes and proteins according to atherosclerosis mechanism. A follow-up analysis was establishing drug-compound-disease-target network. The potential targets were analyzed for protein interactions, and gene enrichment analysis was carried out by GO and KEGG. Molecular docking was carried out between characteristic ingredients of saffron and its key targets. RESULTS: A total of 5 effective components and 272 genes were screened in saffron used oral bioavailability (OB)>30% and drug likeness (DL)>0.18 as the screening conditions. 26 targets of multiple compounds acting together and 50 targets of a single compound were screened from drug-compound-disease-target network. 19 targets, 99 enrichment results and 116 pathways were screened by protein interactions, GO and KEGG gene enrichment analysis respectively. Molecular docking results showed that all 5 active components could be bind with spontaneously VCAM-1 or eNOS, which are representative proteins of fluid shear stress and atherosclerosis pathway. Isorhamnetin had the lowest binding energy with VCAM-1, and kaempferol had the lowest binding energy with eNOS. CONCLUSION: The results preliminarily verified the main activity components and pharmacology mechanism in saffron and provided a good foundation for further study on the antiatherosclerotic mechanism of saffron.

Application of ADaM in safety analysis of bioequivalence trail of generic drugs

ZHU Tianyi, CAI Jingjing, HUANG Jiajun, GENG Zheng, ZHAO Yang, LOU Donghua, YU Hao, BAI Jianling

2020, 25(6):  658-663.  doi:10.12092/j.issn.1009-2501.2020.06.008

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AIM: To promote the Clinical Data Inter-change Standards Consortium (CDISC) standard in clinical trials and promote the standardization of clinical trial data. METHODS: To combine the implementation guide of Analysis Data Model (ADaM) and common problems of actual data, and to introduce the application of analytical data model ADaM in the safety of bioequivalence trails of generic drugs. RESULTS: For different types of clinical trial data, according to various situations that may occur, a safety analysis data set that meets the standards was generated. CONCLUSION: Under the background of the continuous development of generic drugs in China and the low degree of standardization of clinical trial data, the use of CDISC standards in clinical research can promote the standardization of clinical trial data, and can also shorten the time of statistical analysis and accelerate the process of drug development.

Association between the polymorphism of PNPLA2 gene and the risk of ischemic stroke in type 2 diabetic patients in Chinese Han Population

ZHAO Hailing, ZHANG Haojun, ZHAO Tingting, YAN Meihua, DONG Xi, MA Liang, LI Ping

2020, 25(6):  664-669.  doi:10.12092/j.issn.1009-2501.2020.06.009

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AIM: To investigate the association between the polymorphism of the fatty triglyceride lipase gene (PNPLA2) rs1138693 (T>C) and the risk of ischemic stroke in type 2 diabetic patients in China. METHODS: A total of 368 Chinese patients with type 2 diabetes mellitus (T2DM) (139 T2DM ischemic stroke patients and 229 T2DM non-ischemic stroke patients were included as the control group) were included in this case-control study. PNPLA2 rs1138693 (T>C) was genotyped by real-time polymerase chain reaction (PCR) and statistically analyzed by SPSS 20.0. RESULTS: Significant differences were observed in age, sex, blood pressure and homocysteine levels between the control group and the ischemic stroke group (P<0.05). The CC genotype frequency and C allele frequency of PNPLA2 rs1138693 in the ischemic stroke group were significantly lower than those in the control group (genotype frequency: P=0.033; allele frequency: P=0.011). Logistic regression analysis revealed that allele C of PNPLA2 rs1138693 was a protective factor for progression to ischemic stroke in T2DM patients under the additive, dominant and recessive genetic models (P<0.05). CONCLUSION: The PNPLA2 gene rs1138693 is related to the susceptibility of Chinese T2DM patients to ischemic stroke, and the T2DM patients with allele C of rs1138693 are less likely to develop ischemic stroke.

Metformin combined with glucocorticoid in the treatment of SLE patients with IGT

LI Guinv, REN Shaolin, SHEN Ruiming, JI Yongneng, CAI Cairong, SU Ruo

2020, 25(6):  670-676.  doi:10.12092/j.issn.1009-2501.2020.06.010

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AIM: To investigate the clinical curative effect of metformin combined with glucocorticoids in the treatment of patients with systemic lupus erythematosus (SLE) complicated with impaired glucose tolerance (IGT) and the effect on islet function and Th17/Treg cell imbalance. METHODS: Eighty-four patients with SLE complicated with IGT were randomly divided into the combined group and the control group with 42 cases in each group. All of them were given life and diet guidance. The control group was treated with glucocorticoids while the combined group was treated with metformin combined with glucocorticoids. One month later, the curative effect was observed, and islet function and Th17/Treg cell imbalance were evaluated. RESULTS: The total response rate of the combined group was significantly higher than that of the control group (90.48% vs. 71.43%, P<0.05). The SLE activity index score and the erythrocyte sedimentation rate (ESR) [(2.6±0.3) points, (18±4) mm/h] were significantly lower than those in the control group [(3.9±0.8) points, (23±4) mm/h] (P<0.05). Fasting blood glucose (FBG), fasting insulin (Fins), steady-state model-insulin resistance index (HOMA-IR) and islet β-functioning cell index (HOMA-β) in the combined group were significantly improved after treatment (P<0.05). There were statistically significant differences between the two groups (P<0.05). The proportion of NGT in the combined group was significantly higher than that in the control group (73.81% vs. 30.95%, P<0.05). The ratios of Th17 and Treg cells in the combined group were (6.2±0.9) /μL and (31±7) /μL, and Th17/Treg was (0.20±0.05). Compared with the control group [(7.4±1.3) /μL, (28±7) /μL, (0.26±0.06)], there were statistically significant differences (P<0.05). The SLE activity index scores after treatment were significantly correlated with HOMA-IR, HOMA-β and Th17 cells, Treg cells, Th17/Treg (P<0.05). Besides, HOMA-IR and HOMA-β were significantly correlated with Th17 cells, Treg cells and Th17/Treg (P<0.05). The adverse reactions in both groups were mild, and there was no statistically significant difference in the incidence (P>0.05). CONCLUSION: Metformin combined with glucocorticoids is effective in the treatment of SLE with IGT. The treatment can control disease activity, lower blood glucose levels, improve islet function and correct Th17/Treg cell imbalance with high safety.

Research progress on microRNAs in Huntington's disease

JIANG Bingbing

2020, 25(6):  677-685.  doi:10.12092/j.issn.1009-2501.2020.06.011

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Huntington's disease (HD) is a monogenic genetic disease of neurodegenerative disorders caused by repeated amplification of CAG trinucleotides in the first exon of the Huntingtin gene (HTT), and there are no treatments which could forestall or slow Huntington's disease. The protein product encoded by HTT is called huntingtin (Htt). The mutated huntingtin protein (mHtt) is easy to form aggregation which is toxic, leading to a series of cytological abnormalities and neuronal dysfunction. MicroRNA (miRNA) plays an important role in the post-transcriptional regulation of genes whose expression is related to the pathological process of Huntington's disease. miRNA is becoming the promising biomarker for the treatment of HD. Recent studies on the regulation of specific miRNAs in HD and the prediction of their target genes may provide a potential role for the treatment of HD. This review highlights the research progress on miRNAs in the occurrence of HD.

Advances in study of phase II metabolic enzyme expression and activity under diseases status

ZHANG Yu, PENG Ying, WANG Guangji, SUN Jianguo

2020, 25(6):  686-700.  doi:10.12092/j.issn.1009-2501.2020.06.012

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Phase II metabolism is generally considered to be a process of detoxification and inactivation. The enzymatic binding reaction plays a very important role in the process of drug metabolism and detoxification. Under disease status, the expression and activity of drug phase II metabolic enzymes will also change. The effects of disease on human drug metabolism enzymes may be isozyme selective. Studying the changes of phase II metabolic enzymes under disease status is helpful for understanding the regulation mechanism of phase II metabolic enzymes, and has an important role in further research to guide clinical rational drug usage and disease prevention and treatment. This article reviewed the distribution and function of phase II metabolic enzymes, and described their changes in expression/activity in liver disease, digestive tract disease, diabetes, cancer, neurodegenerative disease, glynecological disease and cardiovascular disease. The changes and causes of various phase II metabolizing enzymes under different disease and disease progression were also discussed.

Progress in the development of baicalein and its clinical pharmacology study

SHAN Hui, DU Yinxiao, BAI Hequn, CHEN Junxia, HE Xiaolin, WANG Qian, HU Zijian, LV Cheng, CHEN Xiaoping

2020, 25(6):  701-708.  doi:10.12092/j.issn.1009-2501.2020.06.013

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The 2019 new coronavirus pneumonia (COVID-19) caused by the new coronavirus (SARS-Cov-2) infection has become a global pandemic, and currently there is a lack of specific antiviral drugs. Traditional Chinese medicine plays a critical role in the treatment of COVID-19. Scutellaria baicalensis is an important component of the Qingfei Paidu decoction recommended in the Chinese National Health Commission's Treatment Regimen and Wuhan Xiehe No.2 and No.3 prescriptions as well. Baicalein is the main ingredient in Scutellaria baicalensis, and has various pharmacological effects such as antiviral, antibacterial, antiallergic, and immunomodulatory activities, showing a broad prospect in new drug development. This article systemically reviewed the recent progress in the preclinical and clinical studies, potential drug interactions, and other aspects of baicalein, which will help further development and clinical application of the drug.

Effects of dietary vitamin K on the stability of warfarin anticoagulation therapy

ZHAI Yu, YANG Jin

2020, 25(6):  709-715.  doi:10.12092/j.issn.1009-2501.2020.06.014

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Change in dietary vitamin K intake is one of the main causes of abnormal fluctuations in international standardized ratio (INR) of patients on warfarin therapy. Advice from clinicians on how to manage vitamin K intake for patients has been vague. In the past, patients were often told to restrict or avoid vitamin K-rich foods including leafy greens during anticoagulation therapy, which could lead to lower vitamin K intake. Evidence-based studies in recent years have found that instability of warfarin therapy is associated with low intake of vitamin K. A stable and relatively higher daily intake of vitamin K (>100 μg/d) can reduce unexplained intra-individual variability in response to warfarin, and thus reduce abnormal fluctuations in INR and improve the stability of anticoagulation therapy.

Therapeutic drugs and treatment of SARS-CoV-2

HAO Yuqi, XIAO Yao, WANG Qian, JIANG Xingxu

2020, 25(6):  716-720.  doi:10.12092/j.issn.1009-2501.2020.06.015

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Novel coronavirus pneumonia caused by the SARS-CoV-2 appeared in Wuhan, China in December 2019. The virus spread rapidly across the country and resulted in the infection of more than 80000 people by March 8,2020. This paper introduces the data of tested drugs in vitro, in animal and in clinical trials marketed and in research, in hoping of providing reference for the prevention and control of SARS-CoV-2.