Korean Journal of Physiology & Pharmacology最新文献

{"title":"Eupatilin alleviates right ventricular fibrosis in rats with pulmonary hypertension induced by monocrotaline.","authors":"Tonggang Zhu, Xue Xiao, Xue Li, Zhenkun Liu","doi":"10.4196/kjpp.24.397","DOIUrl":"https://doi.org/10.4196/kjpp.24.397","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is referred to as a tumor of the cardiovascular system and is a major cause of death. It is urgent to develop safe and effective drugs to combat PAH. Eupatilin, a flavonoid extracted from Artemisia, has multiple pharmacological activities. However, the role of Eupatilin in PAH-induced right heart failure is not clear. This study was aimed to investigate the effects of Eupatilin on the PAH <i>via</i> monocrotaline (MCT)-induced rat models and platelet-derived growth factor-BB (PDGF-BB)-induced pulmonary artery smooth muscle cell (PASMC) model. We found Eupatilin inhibits PDGF-BB-induced proliferation of PASMCs <i>in vitro</i>. In addition, Eupatilin affects pulmonary blood flow and right ventricular function induced by MCT in rats. We further revealed Eupatilin alleviates pulmonary artery remodeling induced by MCT. Also, it alleviates myocardial fibrosis induced by MCT. Mechanically, Eupatilin inhibits the JNK/p38 MAPK pathway. Collectively, Eupatilin alleviates MCT-induced pulmonary vascular remodeling as well as right ventricular hypertrophy <i>via</i> JNK/p38 MAPK pathway and could serve as a promising drug to combat PAH.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.","authors":"Giang-Huong Vu, Byeong Hwa Jeon, Cuk-Seong Kim","doi":"10.4196/kjpp.25.236","DOIUrl":"https://doi.org/10.4196/kjpp.25.236","url":null,"abstract":"<p><p>Diabetes mellitus is a major global health concern associated with micro-and macrovascular complications. Among the diverse mechanisms that contribute to vascular dysfunction in diabetes, endothelial to mesenchymal transition (EndMT) has emerged as a key pathological process. EndMT involves the loss of endothelial cell characteristics and the acquisition of mesenchymal features, resulting in impaired endothelial function, increased fibrosis, and inflammation. In addition to findings from preclinical models, recent human studies support the clinical relevance of EndMT. This review summarizes the molecular mechanisms governing EndMT, including key signaling pathways such as TGF-β, Notch, and Wnt, and examines how environmental, metabolic, and inflammatory cues influence this process. Furthermore, we discuss the maladaptive role of EndMT in diabetic complications, including nephropathy, retinopathy, atherosclerosis, and impaired wound healing, highlighting recent advances in anti-EndMT therapies and the clinical implications. Understanding the mechanisms of EndMT in the diabetic milieu may reveal novel therapeutic targets for preventing or reversing diabetic vascular diseases.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poricoic Acid A attenuated TGF-β1-induced epithelial-mesenchymal transition in renal tubular epithelial cells through SPRY2/ERK signaling pathway.","authors":"Ming Xiang, Haiying Chen, Xiangdong Lin","doi":"10.4196/kjpp.24.384","DOIUrl":"https://doi.org/10.4196/kjpp.24.384","url":null,"abstract":"<p><p>The progression of renal fibrosis is difficult to reverse, and Poria cocos, one of the main components of Wenyang Zhenshuai Granules, has been shown to be crucial to the development of the epithelial-mesenchymal transition (EMT). This study aimed to examine the molecular mechanism by which Poricoic Acid A (PAA) inhibited the advancement of EMT in renal tubular epithelial (RTE) cells. The protein levels of sprouty RTK signaling antagonist 2 (SPRY2) extracellular regulated protein kinases (ERK), and p-ERK were measured. The EMT progression of RTE cells was evaluated by a series of experiments. The regulatory relationship of PAA to SPRY2 was determined by cycloheximide, molecular docking and drug affinity target stability and immunoprecipitation. The overexpression of SPRY2 or PAA intervention suppressed the HK-2 and NRK-52E cell's viability, proliferation and migration ability of TGF-β1-induced while raising the levels of E-cadherin and decreasing those of collagen I, collagen III, Fibronectin1, α-SMA, Vimentin, ZEB1, Twist, Snail and Slug. PAA was able to be combined with SPRY2 protein. Besides, we found that PAA intervention increased the stability of SPRY2 through the ubiquitin-proteasome pathway, did not affect ERK levels, and reduced the levels of p-ERK. Finally, we found that inhibiting SPRY2 negated the beneficial effect of PAA on TGF-β1-stimulated RTE cells. PAA alleviated the EMT of RTE cells by modulating the SPRY2/ERK pathway.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemistepsin A induces apoptosis by modulating the reactive oxygen species-dependent PI3K/Akt signaling pathway in human lung carcinoma A549 cells.","authors":"So Young Kim, Gi-Young Kim, Yung Hyun Choi","doi":"10.4196/kjpp.25.044","DOIUrl":"10.4196/kjpp.25.044","url":null,"abstract":"<p><p>Hemistepsin A is a sesquiterpene lactone isolated from plants of the family. Recently, this compound was reported to be a bioactive compound that is beneficial for numerous health problems without side effects; however, its effect on lung cancer cells has not yet been studied. Therefore, in this study, we investigated the anticancer activity of hemistepsin A in human lung carcinoma A549 cells. This study showed that treatment with hemistepsin A induces apoptosis by activating caspase cascade and reducing the expression of inhibitors of apoptotic protein family members. Additionally, hemistepsin A disrupted mitochondrial integration by altering the levels of Bcl-2 family proteins to increase the cytoplasmic release of cytochrome c. Moreover, hemistepsin A reduced the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, and pretreatment with a PI3K inhibitor markedly augmented the cytotoxic effect of hemistepsin A on A549 cells. Furthermore, hemistepsin A significantly enhanced the production of intracellular and mitochondrial reactive oxygen species (ROS), whereas ROS scavengers restored the reduced viability by attenuating DNA damage and apoptosis by blocking the hemistepsin A-mediated inactivation of the PI3K/Akt pathway. Our findings demonstrate that hemistepsin A induces apoptosis in A549 cells by generating ROS, which subsequently inhibits the PI3K/Akt pathway, suggesting that ROS generation is involved as an early inducer of hemistepsin A-mediated anticancer activity.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"625-636"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA circAtxn10 regulates skeletal muscle cell differentiation by targeting miR-143-3p and Chrna1.","authors":"Nakwon Choe, Anna Jeong, Hosouk Joung, Dongtak Jeong, Young-Kook Kim, Hyun Kook, Duk-Hwa Kwon","doi":"10.4196/kjpp.25.046","DOIUrl":"10.4196/kjpp.25.046","url":null,"abstract":"<p><p>Skeletal muscle differentiation is a complex process regulated by a network of genes and transcription factors. Recent studies have revealed the roles of circular RNAs (circRNAs) and microRNAs (miRNAs) in modulating gene expression during myogenesis. In this study, we focused on the functional interplay between circAtxn10, miR-143-3p, and the nicotinic acetylcholine receptor subunit alpha 1 (Chrna1) in skeletal muscle differentiation. Our results demonstrate that circAtxn10 expression increases during myogenic differentiation and acts as a sponge for miR-143-3p through direct binding. We identified Chrna1 as a direct target of miR-143-3p through three binding sites in its 3'-UTR and showed that both miR-143-3p mimic and Chrna1 knockdown significantly impair myogenesis. Notably, Chrna1 overexpression dramatically enhanced myogenic marker expression and myotube formation. Our findings establish a regulatory axis involving circAtxn10, miR-143-3p, and Chrna1 that plays a critical role in modulating skeletal muscle differentiation, providing new insights into the complex molecular mechanisms regulating myogenesis.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"637-648"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory action of citronellol on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in juvenile mice.","authors":"Thi Quy Nguyen, Thi Quynh Nhu Tran, Seon Hui Jang, Seon Ah Park, Seong Kyu Han","doi":"10.4196/kjpp.25.039","DOIUrl":"10.4196/kjpp.25.039","url":null,"abstract":"<p><p>The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) serves as the primary relay point for orofacial nociceptive inputs transmitted <i>via</i> thin myelinated Aδ and unmyelinated C primary afferent fibers. Citronellol is a monoterpenoid alcohol found in the essential oil of various medicinal plants, such as <i>Cymbopogon citratus</i>. It has been shown to be able to alleviate orofacial pain. However, the precise mechanism by which citronellol modulates SG neurons in the Vc remains unclear. To investigate this, the whole-cell patch-clamp technique was used to examine antinociceptive effects of citronellol on SG neurons in the Vc of mice. In a high-chloride pipette solution, citronellol consistently induced inward currents which persisted even in the presence of tetrodotoxin (a voltage-gated Na⁺ channel blocker), 6-cyano-7-nitroquinoxaline-2,3-dione (a non-<i>N</i>-methyl-d-aspartate glutamate receptor antagonist), and DL-2-amino-5-phosphonopentanoic acid (an <i>N</i>-methyl-d-aspartate receptor antagonist). Nevertheless, citronellol-induced inward currents were partially inhibited by picrotoxin, a GABA_A receptor antagonist, or strychnine, a glycine receptor antagonist. Citronellol-induced inward currents were almost fully blocked when both strychnine and picrotoxin were applied together. In addition, citronellol enhanced both GABA-induced inward currents and glycine-induced inward currents. These findings suggest that citronellol can mediate inhibitory effects of GABA and glycine on SG neurons in the Vc and serve as a potential herbal treatment for orofacial pain.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"603-611"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tie2 activator 4E2 ameliorates diabetic nephropathy and synergizes with dapagliflozin in a mouse model.","authors":"Da Som Jeong, Soo Min Ko, Ji-Young Lee, Hyo-Jeong Han, Yerin Lee, Weon Sup Lee, Eun-Ah Lee, Woo-Chan Son, Jinho Shin","doi":"10.4196/kjpp.24.424","DOIUrl":"10.4196/kjpp.24.424","url":null,"abstract":"<p><p>Diabetic nephropathy (DN), a primary cause of end-stage renal disease, stems from hyperglycemia-induced vascular dysfunction and aberrant angiogenesis. Sodium-glucose cotransporter 2 inhibitors, such as dapagliflozin, improve glycemic control and provide renal protection yet fall short of fully halting DN progression. This study explores 4E2, a Tie2 receptor activator that mimics angiopoietin-1 to stabilize the vascular endothelium, as a novel DN therapy-both independently and in combination with dapagliflozin. In a streptozotocin (STZ)-induced DN mouse model (DBA/2J strain), male mice were treated with weekly intravenous 4E2, daily oral dapagliflozin, or a combination of both for 4 weeks following STZ administration. Dapagliflozin primarily reduced fasting blood glucose with modest renoprotective effects, whereas 4E2 significantly lowered kidney weight, blood urea nitrogen, and urinary albumin while elevating serum albumin, indicating greater renal protection. Histological analysis showed that 4E2 more effectively attenuated glomerular hypertrophy and lesions compared to dapagliflozin. Immunohistochemistry revealed that 4E2 markedly increased VE-cadherin and CD31 expression while decreasing PDGFR-β, reflecting enhanced endothelial stability and reduced vascular remodeling through Tie2-mediated mechanisms. Combination therapy synergistically enhanced these outcomes, achieving superior reductions in glucose levels, glomerular damage, and vascular pathology compared to either treatment alone. In contrast to anti-VEGF therapies, which can worsen proteinuria, 4E2-mediated Tie2 activation normalizes vascular stability without disrupting physiological angiogenesis, providing a safer therapeutic option. These findings establish 4E2 as a promising treatment for DN, especially when combined with dapagliflozin, by leveraging Tie2-driven stabilization and synergistic benefits to meet this critical unmet need.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"613-623"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144709957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Agmatine decreases long-term potentiation <i>via</i> α2-adrenergic receptor and imidazoline type 1 receptor in the hippocampus.","authors":"Wonseok Chang, Jihua An, Sang Hyun Jang, Moonil Kim, Sun Seek Min","doi":"10.4196/kjpp.24.399","DOIUrl":"10.4196/kjpp.24.399","url":null,"abstract":"<p><p>Agmatine, a decarboxylation product of L-arginine, has been proposed as a novel neurotransmitter/neuromodulator with diverse neuroprotective and antidepressant-like effects. Although its therapeutic potential has been explored, the precise mechanisms by which agmatine modulates synaptic transmission and plasticity in the hippocampus remain unclear. In this study, we investigated the effects of agmatine on the induction and maintenance of long-term potentiation (LTP) in the CA1 region of mouse hippocampal slices, its ability to counteract amyloid-β (Aβ1-42)-induced LTP impairment, and the receptor systems involved. Bath application of agmatine significantly suppressed the maintenance phase of LTP. Notably, agmatine reversed Aβ-induced deficits in LTP, suggesting a protective effect against synaptic dysfunction. Pharmacological experiments demonstrated that these effects were mediated <i>via</i> α2-adrenergic and imidazoline type I receptors. Paired-pulse facilitation and input-output analyses revealed that agmatine did not alter presynaptic release probability but selectively modulated postsynaptic transmission, particularly under AMPA receptor blockade, indicating a potential regulation of NMDA receptor-mediated signaling. Together, these findings suggest that agmatine modulates hippocampal synaptic plasticity through receptor-specific, postsynaptic mechanisms, and highlight its potential as a therapeutic agent against synaptic impairments in neurodegenerative diseases.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"593-601"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144735523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of β-adrenoceptor antagonist and 5-HT_1A and 5-HT_1B receptor antagonist alprenolol on human Kv1.3 currents.","authors":"Eunseo Kim, Su-Hyun Jo","doi":"10.4196/kjpp.25.098","DOIUrl":"10.4196/kjpp.25.098","url":null,"abstract":"<p><p>Alprenolol is a nonselective β-adrenoceptor antagonist used in treating cardiovascular diseases by stabilizing elevated heart rates and myocardial contractility through the inhibition of sympathetic nerve transmissions alongside its role as an antagonist of 5-HT_1A and 5-HT_1B receptors. This study aimed to examine whether alprenolol can affect human Kv1.3 channel (hKv1.3) currents, which contribute to the proliferation and activation of T lymphocytes by regulating the driving force of Ca²⁺ influx. We investigated the acute effects of alprenolol on hKv1.3 channel currents using two-microelectrode voltage clamp recordings in <i>Xenopus</i> oocytes. Alprenolol exhibited concentration-dependent biphasic effects on hKv1.3 currents: it increased the current amplitudes at 1-100 μM but decreased them at 300-1,000 μM during a +50 mV depolarization step. A significant difference was found in alprenolol's effects on the peak and steady-state currents after 6 min of treatment with 10 μM, 50 μM, and 100 μM and 12 min of treatment with 10 μM and 50 μM. Furthermore, alprenolol affected the time constants of intrinsic inactivation and ultrarapid activation. However, no significant changes in <i>V_1/2</i> and <i>k</i> value were found for steady-state activation and inactivation curves, except for the <i>k</i> value between 50 μM and 1,000 μM of the inactivation curve. At 1,000 μM, alprenolol suppressed hKv1.3 currents more rapidly during 5 sec inter-stimulus intervals compared to 15 sec intervals, indicating use-dependent blockade. Therefore, the effects of alprenolol on the biphasic and various biophysical properties of hKv1.3 channels could cause drug concentration-dependent changes in immune function.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"649-658"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144555821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phytochemicals as promising agents in Axl-targeted cancer treatment.","authors":"ChuHee Lee","doi":"10.4196/kjpp.25.006","DOIUrl":"10.4196/kjpp.25.006","url":null,"abstract":"<p><p>Axl, a receptor tyrosine kinase, plays a critical role in various cellular processes, such as survival, proliferation, migration, and immune response regulation. Dysregulation of Axl, particularly its overexpression and activation, is implicated in several cancers, where it has been found to facilitate tumor growth, metastasis, and the development of resistance to chemotherapy. Consequently, the inhibition of Axl has garnered significant interest as a potential strategy for cancer treatment. Natural compounds, known for their structural diversity and inherent bioactivity, are a valuable resource for drug discovery. These compounds offer a vast array of chemical structures that can serve as potential inhibitors of Axl, thereby providing novel approaches to modulate its activity. Researchers have identified various natural compounds that exhibit inhibitory effects on Axl, which underscore their potential for developing effective therapies. This review strives to provide a comprehensive overview of natural compounds that have been identified as Axl inhibitors. It will examine the mechanisms through which these natural compounds exert their inhibitory effects on Axl and discuss their potential applications in therapeutic settings. By compiling and analyzing existing research, this review seeks to advance the understanding of natural compounds as viable candidates in the development of effective Axl-targeted therapies, ultimately contributing to improved outcomes in diseases marked by Axl dysregulation.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"533-545"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}