Annals of Translational Medicine
·
2020
·
IF 3.297
Ying Li,Mingzhu Shan,Shihui Li,Yuechen Wang,Huan Yang,Ying Chen,Bing Gu,Zuobin Zhu
Background Candidiasis has long been a threat to human health, but cytotoxicity and resistance always block the usefulness of antifungal agents. The ability to switch between yeast and hypha is one of the most discussed virulence trait attributes of the human pathogenic fungus Candida albicans . The morphological transition provides a novel target for developing antifungal drugs. The aim of the present study was to explore the activity and mechanism of teasaponin (TS), a generally regarded as safe natural product, in inhibiting filamentation of C. albicans , hoping to provide an experimental basis for its clinical application. Methods The effect of TS on filamentation and biofilm formation of C. albicans was evaluated by XTT reduction assay and microscopy. The level of intracellular cAMP was measured to further explore the underlying mechanism. In addition, cytotoxicity of TS was evaluated by using MTT assay in vitro and Caenorhabditis elegans model in vivo . The potential of TS-resistance induction was tested by a serial passage experiment. Results TS displayed a moderate antifungal activity against the wild type, efflux pump mutant and multi-resistance C. albicans strains, and could effectively retard filamentation and biofilm formation with a low MIC value. Further mechanism investigation revealed that the reduced cAMP level inhibited filamentation and biofilm formation. In addition, TS showed no significant cytotoxicity in vitro or in vivo , and had little potential to develop resistance during long-time induction. Conclusions Our work evaluated the antifungal activity of TS against filamentation and biofilms formation of C. albicans and disclosed the underlying mechanism, which might provide useful clues for the potential clinical application of TS in fighting clinical fungal infections by targeting the virulence factors.
研究领域:
微生物学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
Anti-Cancer Agents in Medicinal Chemistry
·
2024
·Vol. 24
·期 5
·348-357
·
IF 2.6
Fan Ning,Zhang Lixiu,Wang Zhiping,Ding Hui,Yue Zhongjin
Background: Bladder cancer is the most common malignant tumor of the urinary system. Nevertheless, current therapies do not provide satisfactory results. It is imperative that novel strategies should be developed for treating bladder cancer. Objectives: To evaluate the effect of
a broad-spectrum anti-parasitic agent, Ivermectin, on bladder cancer cells in vitro and in vivo. Methods: CCK-8 and EdU incorporation assays were used to evaluate cell proliferation. Apoptosis was detected by flow cytometry, TUNEL assay, and western blotting. Flow cytometry
and DCFH-DA assay were used to analyze the reactive oxygen species (ROS) levels. DNA damage was determined by Neutral COMET assay and γ H2AX expression. Proteins related to apoptosis and DNA damage pathways were determined by WB assay. Xenograft tumor models in nude mice were used to
investigate the anti-cancer effect of Ivermectin in vivo. Results: Our study showed that in vitro and in vivo, Ivermectin inhibited the growth of bladder cancer cells. In addition, Ivermectin could induce apoptosis, ROS production, DNA damage, and activate ATM/P53
pathwayrelated proteins in bladder cancer cells. Conclusion: According to these findings, Ivermectin may be a potential therapeutic candidate against bladder cancer due to its significant anti-cancer effect.
研究领域:
肿瘤学
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药理学
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分子生物学
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癌症研究
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PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2026
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IF 3.2
Ye Yuan,Chen Chen,Shengjie Zeng,Lianju Shen,Qing Jiang,Junke Wang
DBP exposure impaired BTB integrity in prepubertal male mice. • MBP induced G1-phase arrest, apoptosis, and DNA damage in Sertoli cells. • MBP impaired Sertoli cell viability and cytoskeletal organization through activation of the ATM/Chk2/p53 pathway. Dibutyl phthalate (DBP) has been recognized as an endocrine disrupting chemical, which poses significant threats to male reproductive health, though its precise mechanism of testicular toxicity has not been fully clarified. We combined in vivo and in vitro experiments with transcriptome sequencing to investigate the toxicity of DBP and its active metabolite monobutyl phthalate (MBP) in prepubertal male mice and Sertoli cells, and explored the underlying molecular mechanisms. The results showed that DBP affected testicular development and disrupted the blood-testis barrier (BTB) in mice. Through bioinformatic analysis, we validated that MBP promoted G1 phase cell cycle arrest, apoptosis, and DNA damage in Sertoli cells. Furthermore, the increased expression of p -ATM, p -Chk2, p-p53 indicated that the ATM/Chk2/p53 signaling pathway was activated upon MBP treatment. Inhibition of p53 or ATM expression partially reversed the pro-apoptotic and cell cycle-arrested phenotypes, whereas p53 overexpression reverted these phenotypic abnormalities. These findings indicated that prepubertal DBP exposure impaird BTB integrity and induced DNA damage in association with pathological activation of the ATM/Chk2/p53 signaling pathway, thereby contributing to Sertoli cell apoptosis and proliferative arrest. Download: Download high-res image (283KB) Download: Download full-size image
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PubMed
高影响因子
Acta Pharmaceutica Sinica B
·
2021
·
IF 11.614
Fangfang Wang,Sora Jin,Franklin Mayca Pozo,Danmei Tian,Xiyang Tang,Yi Dai,Xinsheng Yao,Jinshan Tang,Youwei Zhang
DNA damage response (DDR) is a highly conserved genome surveillance mechanism that preserves cell viability in the presence of chemotherapeutic drugs. Hence, small molecules that inhibit DDR are expected to enhance the anti-cancer effect of chemotherapy. Through a recent chemical library screen, we identified shikonin as an inhibitor that strongly suppressed DDR activated by various chemotherapeutic drugs in cancer cell lines derived from different origins. Mechanistically, shikonin inhibited the activation of ataxia telangiectasia mutated (ATM), and to a lesser degree ATM and RAD3-related (ATR), two master upstream regulators of the DDR signal, through inducing degradation of ATM and ATR-interacting protein (ATRIP), an obligate associating protein of ATR, respectively. As a result of DDR inhibition, shikonin enhanced the anti-cancer effect of chemotherapeutic drugs in both cell cultures and in mouse models. While degradation of ATRIP is proteasome dependent, that of ATM depends on caspase- and lysosome-, but not proteasome. Overexpression of ATM significantly mitigated DDR inhibition and cell death induced by shikonin and chemotherapeutic drugs. These novel findings reveal shikonin as a pan DDR inhibitor and identify ATM as a primary factor in determining the chemo sensitizing effect of shikonin. Our data may facilitate the development of shikonin and its derivatives as potential chemotherapy sensitizers through inducing ATM degradation.
研究领域:
癌症生物学
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药理学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
International Journal of Biological Sciences
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2021
·
IF 6.582
Dian Bao,Hua Su,Chun-Tao Lei,Hui Tang,Chen Ye,Wei Xiong,Fang-Fang He,Ji-Hong Lin,Hans-Peter Hammes,Chun Zhang
Rationale: Focal segmental glomerulosclerosis (FSGS) is characterized by the dysfunction of “post-mitotic” podocytes. The reentry of podocytes in the cell cycle will ultimately result in cell death. Mitotic arrest deficient 2-like protein 2 (MAD2B), an inhibitor of anaphase-promoting complex (APC)/cyclosome, precisely controls the metaphase to anaphase transition and ordered cell cycle progression. However, the role of MAD2B in FSGS podocyte injury remains unknown. Methods: To explore MAD2B function in podocyte cell cycle reentry, we used conditional mutant mice lacking MAD2B selectively in podocytes in ADR-induced FSGS murine model. Additionally, KU-55933, a specific inhibitor of ataxia-telangiectasia mutated (ATM) was utilized in vivo and in vitro to explore the role of ATM in regulating MAD2B. Results: The expression of MAD2B in podocytes was dramatically increased in patients with FSGS and ADR-treated mice along with podocyte cell cycle reentry. Podocyte-specific knockout of MAD2B effectively attenuated proteinuria, podocyte injury, and prevented the aberrant cell cycle reentry. By bioinformatics analysis we revealed that ATM kinase is a key upstream regulator of MAD2B. Furthermore, inhibition of ATM kinase abolished MAD2B-driven cell cycle reentry and alleviated podocyte impairment in FSGS murine model. In vitro studies by site-directed mutagenesis and immunoprecipitation we revealed ATM phosphorylated MAD2B and consequently hampered the ubiquitination of MAD2B in a phosphorylation-dependent manner. Conclusions: ATM kinase-MAD2B axis importantly contributes to the cell cycle reentry of podocytes, which is a novel pathogenic mechanism of FSGS, and may shed light on the development of its therapeutic approaches.
研究领域:
肾病学
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细胞生物学
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分子生物学
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DOI
PubMed
高影响因子
COMBUSTION AND FLAME
·
2018
·
IF 4.494
Guoqing Wang,Yuyang Li,Wenhao Yuan,Yizun Wang,Zhenbiao Zhou,Yingzheng Liu,Jianghuai Cai
Bio-butanol is an important alternative fuel and has many advantages in engine combustion . In the present work, laminar flame propagation of n- butanol/air and n- butanol/(14% O 2 /86% He) mixtures was investigated using a constant-volume combustion vessel at the unburnt temperature of 423 K, initial pressures of 1–20 atm and a series of equivalence ratios. Flame instabilities of n -butanol, including cellular instability and pulsating instability, were studied based on flame morphology. The unsteady transition from weak flame to normal flame was investigated based on the flame trajectories and this phenomenon became less perceptible in the flame with stronger combustion intensity and smaller Lewis number. The accelerated laminar burning velocity (LBV), thickened flame thickness, larger Markstein length and Markstein number indicate that the thermal diffusivity of n- butanol/O 2 /He flames are greatly enhanced by helium addition. The smaller densities and lower reactant concentrations result in the smaller laminar burning fluxes of n- butanol/O 2 /He flames than those of n -butanol/air flames. The high temperature kinetic model of n -butanol reported by Cai et al. was further developed with recent theoretical progresses on n -butanol reactions. The updated high temperature model was validated on the present experimental data and a vast amount of previous n -butanol combustion data . Sensitivity analysis was performed using the updated model under wide pressure and equivalence ratio ranges. The similarity in the sensitivities indicates that the sensitive reactions in n- butanol/air flames can be validated by using n- butanol/O 2 /He flames, which greatly compensates the problem that the n- butanol/air flames are susceptible to flame instabilities at high pressures. The weaker pressure dependence of the LBVs of n -butanol/O 2 /He flames indicates that their flame chemistry changes less to resist the pressure variation.
研究领域:
燃烧学
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化学反应动力学
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DOI
高影响因子
Annals of Translational Medicine
·
2022
·Vol. 10
·期 18
·971-971
·
IF 3.616
Shuqi Zhao,Meifeng Chen,Zhu Yu,Thi Thai Hoa Pham,Shutian Mo,Yongfei He,Tianyi Liang,Wenlong Cao,Chuangye Han
BackgroundBreast cancer (BC) is the most common type of cancer affecting females. It is also a leading cause of cancer-related death in women worldwide.MethodsSonodynamic therapy (SDT) is an emerging therapeutic strategy for cancer treatment. SDT ensures non-invasive penetration of deep tumors and results in activation of non-toxic sonosensitizers administered in deep tumor sites to become cytotoxic. It has been reported that 2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD) has a significant anti-tumor effect against various cancer types including BC. However, DMDD is hydrophobic. Therefore, a one-step encapsulation method was used in the current study to construct zeolitic imidazole frameworks-8 (ZIF-8) loaded with DMDD and sonosensitizer chlorin e6 (Ce6). ZIF-8 was further modified by coating it with a biomimetic cell membrane to improve targeted delivery.ResultsIn vitro and in vivo results indicated that the nanomedicines had great biocompatibility properties and targeting ability. The nanocomposite exhibited a higher release rate under an acidic tumor microenvironment. The tumor killing effect of reactive oxygen species (ROS) generated from Ce6 and inhibition of tumor growth was enhanced after ultrasound (US) treatment, which might be caused by the increase in apoptosis rate.ConclusionsThese findings show that the combination of nanomedicine and SDT provides a potential therapeutic method for BC.Keywords: Breast cancer (BC), 2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD), metal-organic framework, sonodynamic therapy, ZIF-8 nanoparticles
研究领域:
肿瘤学
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纳米技术
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药学
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治疗学
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2022
·Vol. 10
·期 20
·1101-1101
·
IF 3.616
Jiangyan He,Yiyuan Zhou,Taiwei Zhang,Yan Zou,Hua Huang
Background Subclinical hypothyroidism (SH) is common during pregnancy. It is not clear whether decidual cells in SH undergo pyroptosis during pregnancy. This study aimed to investigate the possible mechanism of Bushen Antai recipe (BAR) in the treatment of SH in early pregnancy and the relationship between SH during pregnancy and decidual cell pyroptosis through a rat model. Methods A total of 60 female rats were divided into control group, model group, levothyroxine (L-T4) group, low-dose BAR group (6 g/kg), medium-dose BAR group (12 g/kg), and high-dose BAR group (24 g/kg). The control group underwent pseudothyroidectomy, while the remaining groups established nonpregnant SH rat models. Except for the blank control group, rats were successfully established with SH models during pregnancy. The control group and the model group were treated with saline or BAR. The animals were sacrificed 12 hours after the last administration. The levels of serum thyroid-stimulating hormone (TSH), free thyroxine (FT4), interleukin-1β (IL-1β), and interleukin-18 (IL-18) were detected by enzyme-linked immunosorbent assay (ELISA). Western blot was used to detect the expression of decidual nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, Caspase-1, and porin family proteins. Results There was no significant difference in serum FT4 among groups (P>0.05). Compared with the control group, serum TSH, IL-1β, IL-18, and NLRP3, Caspase-1, and gasdermin D (GSDMD) proteins in the decidua of the model group were significantly increased (P<0.05). Compared with the model group, the L-T4 group and the high-dose BAR group could significantly decrease the levels of serum TSH, IL-1β, IL-18, and NLRP3, Caspase-1, and GSDMD in decidual tissue (P<0.05). The medium dose of BAR could significantly decrease the levels of TSH, NLRP3, Caspase-1, and GSDMD (P<0.05), and the low dose group of BAR significantly decreased the levels of TSH, NLRP3, and GSDMD (P<0.05). Among them, the high-dose group of BAR had the best reducing effect on IL-18, NLRP3, Caspase-1, and GSDMD. Conclusions The decidual cells of SH rats in early pregnancy underwent pyroptosis with a high inflammatory response. BAR could improve TSH level in SH during pregnancy, inhibit decidual cell pyroptosis, and reduce the expression of inflammatory factors.
研究领域:
内分泌学
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妇产科学
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药理学
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免疫学
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2021
·
IF 3.932
Rongxue Shao,Changming Li,Yan Chen,Liang Zhang,Hejie Yang,Zhijing Zhang,Jun Yue,Wenshuo Gao,Hang Zhu,Hao Pan,Hui Zhou,Renfu Quan
Background Stem cell transplantation has been increasingly used for spinal cord repair, and some achievements have been made. However, limited stem cell sources as well as immune rejection and ethical issues have restricted its wide application. Therefore, to achieve further breakthroughs regarding the application of stem cell transplantation to treat spinal cord injury (SCI), it is important to develop a stem cell line that can effectively avoid immune rejection and ethical issues. Methods Urine cells (UCs) were induced to differentiate into induced pluripotent stem cells (iPSCs), which then further differentiated into neural stem cells (NSCs). Relevant tests were performed, and three-dimensional (3D) printed scaffolds were prepared. Thirty C57BL/6 mice were divided into 5 groups based on a random number table: a sham group, an SCI group, an SCI + control group, an SCI + siNC group, and an SCI + siGAS5 group (n=6). The latter 4 groups replicated SCI models. Mice in the SCI + control group were transplanted with 3D scaffolds loaded with iPSC-derived NSCs (iPSd-NSCs). Mice in the SCI + siNC group and the SCI + siGAS5 group were transplanted with scaffolds loaded with iPSd-NSCs-siNC and 3D scaffolds loaded with iPSd-NSCs-siGAS5, respectively. Mice in the other groups were injected with the same amount of normal saline. Hematoxylin-eosin staining was used to observe the histopathology of the injured spinal cord, the Basso-Mouse Scale was used to assess the motor function of the hind limbs of the mice, and Western blot was used to detect the expression of apoptosis-related proteins after SCI. Results iPSd-NSCs were successfully induced and differentiated, and 3D printed heparin sulfate-collagen scaffolds were prepared, inside which a 3D loose porous structure was shown by electron microscopy. Morphological observations showed that iPSd-NSC transplantation improved SCI in mice, while GAS5 silencing inhibited the reparative effect of iPSd-NSC transplantation on SCI in mice. Western blot results indicated that iPSd-NSC transplantation significantly increased the expression level of B cell lymphoma/leukemia-2 (Bcl-2) (P<0.01) but decreased the expression levels of Bcl-2 associated X protein, cytochrome C, and cleaved caspase-3 (P<0.001). Conclusions The overexpression of lncRNA-GAS5 can promote spinal cord repair and inhibit neural apoptosis via the transplantation of 3D printed scaffolds loaded with iPSd-NSCs.
研究领域:
神经科学
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干细胞生物学
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组织工程
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2022
·Vol. 10
·期 22
·1239
·
IF 3.616
Yuan Liu,Fuai Lu,Xiaofen Li,Youguo Yang,Jianqing Yang
Background: Pulmonary fibrosis, which is a frequent manifestation of connective tissue disease (CTD), is a leading cause of morbidity and mortality. However, the role of long non-coding ribonucleic acids (lncRNAs) in CTD-associated pulmonary fibrosis requires clarification. This study sought to examine the effects of lnc-NONHSAT071210 on the phenotypes of transforming growth factor β1 (TGFβ1)-treated lung epithelial cells. Methods: The GeneChip was used to identify differentially expressed lncRNAs in CTD-associated pulmonary fibrosis patients. After lnc-NONHSAT071210 was knocked down in the TGFβ1-challenged lung epithelial cells, cell viability, cell cycle, migration, and invasion were estimated by Cell Counting Kit-8 assays, a flow cytometry analysis, wound-healing assays, and transwell assays, respectively. The expression and levels of the fibrosis-associated factors were examined by enzyme-linked immunosorbent assays, RT-qPCR, and western blots. Results: The expression of the top 7 most significantly upregulated lncRNAs in the CTD-associated pulmonary fibrosis patients was depicted in a heat map and examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that the expression of lnc-NONHSAT071210 was significantly increased in the tissues of the CTD-associated pulmonary fibrosis patients (P<0.001). The silencing of Lnc-NONHSAT071210 suppressed proliferation, migration, and invasion in the TGFβ1-exposed alveolar epithelial cells (P<0.001). Conclusions: Thus, lnc-NONHSAT071210 expression was increased in the tissues of the CTD-associated pulmonary fibrosis patients and TGFβ1-treated lung epithelial cells, and TGFβ1-induced lung epithelial cell injury was alleviated by impeding the expression of lnc-NONHSAT071210.
研究领域:
分子生物学
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肺病学
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细胞生物学
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病理学
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2022
·
IF 3.616
Shi-Ji Deng,Jian-Wei Ge,Sheng-Nan Xia,Xin-Xin Zou,Xin-Yu Bao,Yue Gu,Yun Xu,Hai-Lan Meng
Background Neuroinflammation, which is mainly mediated by excessive microglia activation, plays a major role in ischemic stroke. Overactivated microglia secrete numerous inflammatory cytokines, causing excessive inflammatory responses and ultimately exacerbating ischemic brain injury. Hence, compounds that attenuate neuroinflammation could become promising drug candidates for ischemic stroke. Fraxetin has an anti-inflammatory effect in many inflammatory diseases. However, whether it possesses an anti-inflammatory capacity in microglia-mediated neuroinflammation after ischemic brain injury is unknown. Our study aimed to investigate the suppression effect of fraxetin on neuroinflammation in lipopolysaccharide (LPS)-activated microglia and establish whether fraxetin could alleviate ischemic brain injury in a rodent model of ischemic stroke. Methods For the in vitro experiment, primary microglia were obtained from 1-day-old C57/BL6J mice. The cells were activated with LPS and treated with fraxetin at a non-cytotoxic concentration. Real-time PCR, enzyme-linked immunosorbent assays, and immunofluorescence staining were used to evaluate the anti-inflammatory effects of fraxetin. The potential molecular mechanisms were explored and verified through RNA-sequencing analysis, western blotting and real-time PCR. For the in vivo experiment, focal ischemia was induced by middle cerebral artery occlusion (MCAO) in 8-week-old male C57/BL6J mice. Fraxetin (5 mg/kg) or an equal volume of saline was injected into mice intraperitoneally after MCAO, and 2% 2,3,5-triphenyltetrazolium chloride staining was applied to measure infarct volume. Behavioral tests were conducted to measure neurological deficits in the mice. Real-time PCR, western blotting, and immunofluorescence staining were used to examine the expression of inflammatory cytokines and microglia activation in the ischemic penumbra. Results Fraxetin effectively inhibited the expression of proinflammatory cytokines including inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-1 beta, and interleukin-6 in LPS-activated microglia. Fraxetin also suppressed the PI3K/Akt/NF-κB signaling pathway in activated microglia, which contributed to its anti-inflammatory effects. Furthermore, the administration of fraxetin attenuated ischemic brain injury and behavioral deficits after stroke. Finally, fraxetin was found to attenuate the activation of microglia both in vitro and in vivo . Conclusions Our results suggest that fraxetin has a suppression effect on microglia-mediated neuroinflammation, and this effect is associated with the PI3K/Akt/NF-κB signaling pathway. Fraxetin may therefore have potential neuroprotective properties for ischemic stroke.
研究领域:
神经科学
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药理学
·
炎症
·
中风
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2020
·
IF 3.297
Shuang Chen,Mengzhen Li,Wei Jiang,Hao Zheng,Lian-Wen Qi,Shujun Jiang
Background Pharmacological induction of autophagy can protect against acetaminophen (APAP) induced acute liver failure (ALF) by removing APAP adducts (APAP-AD), but its mechanism is not well understood. Hepatoprotective effect of saponins from traditional Chinese medicine has attracted widespread attention from all over the world. The content of saponins in Lonicerae Flos (Shanyinhua in Chinese) is up to 15–25%. Dipsacoside B (DB) is a common bioactive ingredient of different Shanyinhua, but its hepatoprotective effect and mechanism are still unknown. The present investigation aimed to study the benefit of DB in APAP-induced hepatotoxicity mouse model and different cell model. Methods Mice were treated with DB by intraperitoneal injection 1 h before treated with 500 mg/kg APAP, which caused ALF after 4 h. HepG2 cells were treated with DB for 1 h before treated with 10 mM APAP for 12 h. Hepatotoxicity was assessed via ALT and AST. Neuraminidase 1 (Neu1), lysosomal autophagy marker LC3 and P62 were examined by western blot. Neu1 activity was assayed using its substrate 2-(4-methylumbelliferyl)-D-N-acetylneuraminic acid. Apoptosis level was examined by TUNEL and caspase 3 activity. Molecular docking was used to predict the interaction between DB and protein Neu1. Results Our results demonstrated that pretreatment with 0.5 μM DB ( in vitro ) and 50 mg/kg DB ( in vivo ) respectively reversed increased level of AST and ALT induced by APAP. Histopathological examinations showed reduced necrosis and apoptosis in the liver of DB-treated APAP mice. DB promoted the removal of APAP-AD by lysosomal autophagy. These effects were associated with significant decrease in the level of Neuraminidase 1 (Neu1), a negative regulator of lysosomal exocytosis. Molecular docking results showed that DB could bind to Neu1 protein (binding energy =−7.86 kcal/mol). Akt/mTOR-mediated autophagy and inhibition of apoptosis may be the main mechanisms for the hepatoprotective effects of DB in acetaminophen-induced liver injury. Conclusions These data indicate that DB alleviated hepatotoxicity caused by APAP at least in part via Neu1 inhibition, Akt/mTOR pathway is involved in the detoxification effect of DB on acetaminophen-induced hepatotoxicity.
研究领域:
药理学
·
肝病学
·
传统中药
·
分子生物学
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DOI
PubMed
高影响因子
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