PHYTOTHERAPY RESEARCH
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2025
·
IF 6.3
Qing Ning,Yingxue Yue,Xinlian Liu,Wenbo Ji,Qin Zhao,Jing Wang,Zhenhai Zhang
S afe and effective treatments for psoriasis are limited. Anisole is an active ingredient in citrus and basil volatile oils; however, its potential for psoriasis treatment remains unexplored. To investigate the effects and mechanism of anisole transdermal administration as a treatment for psoriasis. Imiquimod (IMQ) was used to establish a C57 mouse psoriasis model. The severity of psoriasis lesions in each group was assessed by evaluating the thickness of skin lesions, erythema, and scales. Pathological changes within the epidermis organization were evaluated via hematoxylin and eosin (H&E) staining using light microscopy. Serum inflammatory factor levels were measured by enzyme-linked immunosorbent assays. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) were performed to analyze the mRNA levels of relevant inflammatory factors and the expression of key proteins at the skin lesion sites in psoriatic mice. In model mice, applying anisole hydrogels significantly reduced the serum levels of pro-inflammatory factors interleukin (IL)-17A, (IL)-23, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ. H&E staining revealed significantly attenuated stratum spinosum thickening and lymphocyte infiltration in the treatment group. RT-qPCR results further demonstrated that the skin tissues from the treatment group exhibited significantly reduced Il1b , Il17a , Il22 , and Tnfa mRNA expression. Western blotting revealed inhibition of the JAK1/STAT3 signaling pathway within anisole-treated psoriatic tissues. Anisole potentially reduces psoriatic-associated inflammation through the JAK1/STAT3 signaling pathway, alleviating IMQ-induced psoriasis.
研究领域:
皮肤病学
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免疫学
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药理学
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产品关联
DOI
PubMed
高影响因子
Journal of Genetics and Genomics
·
2025
·
IF 7.1
Wuming Qin,Xiaobo Yang,Lu Zhang,Linghui Cao,Shi Ouyang,Dafeng Yang,Yangzhao Zhou,Anji Chen,Tao Liao,Xinyu Zhu,Yuting Liu,Wei Tang,Tongtong Ma,Yiyue Tang,Yonghe Ding,Yun Deng
LIM zinc finger domain containing 1 (LIMS1), an evolutionally conserved LIM domain adaptor protein, is implicated in diverse pathologies, including cancer and neurological disorders. However, its roles in cardiac diseases and the underlying mechanisms remain unclear. Here, we explore the functions and mechanisms of LIMS1 in cardiac remodeling and heart failure. We identify the elevated LIMS1 expression in patients with dilated cardiomyopathy (DCM) and murine cardiomyocytes, suggesting that LIMS1 dysregulation contributes to cardiac pathology. Using CRISPR/Cas9 technology, we generate a zebrafish model of lims1 loss-of-function mutant, which exhibits severe cardiac chamber remodeling, systolic dysfunction, and premature mortality, demonstrating the essential role of lims1 in maintaining cardiac integrity. Transcriptomic profiling reveals the activation of the gp130/Jak1/Stat3 signaling in the lims1 -deficient hearts. Strikingly, pharmacological inhibition of Stat3 or c-Fos partially rescues cardiomyopathy phenotypes. Our findings reveal the underlying mechanism of lims1 deficiency-caused heart failure through gp130/Jak1/Stat3 hyperactivation, offering insights into cardiac remodeling and potential therapeutic strategies.
研究领域:
心血管病学
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分子生物学
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遗传学
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DOI
PubMed
高影响因子
Cells
·
2022
·Vol. 11
·期 22
·3588
·
IF 7.666
Tuo Li,Lei Li,Ruilong Peng,Hongying Hao,Hejun Zhang,Yalong Gao,Cong Wang,Fanjian Li,Xilei Liu,Fanglian Chen,Shu Zhang,Jianning Zhang
Background and Purpose: Neuroinflammation has been shown to play a critical role in secondary craniocerebral injury, leading to poor outcomes for TBI patients. Abrocitinib, a Janus kinase1 (JAK1) selective inhibitor approved to treat atopic dermatitis (AD) by the Food and Drug Administration (FDA), possesses a novel anti-inflammatory effect. In this study, we investigated whether abrocitinib could ameliorate neuroinflammation and exert a neuroprotective effect in traumatic brain injury (TBI) models. Methods: First, next-generation sequencing (NGS) was used to select genes closely related to neuroinflammation after TBI. Then, magnetic resonance imaging (MRI) was used to dynamically observe the changes in traumatic focus on the 1st, 3rd, and 7th days after the induction of fluid percussion injury (FPI). Moreover, abrocitinib’s effects on neurobehaviors were evaluated. A routine peripheral blood test was carried out and Evans blue dye extravasation, cerebral cortical blood flow, the levels of inflammatory cytokines, and changes in the numbers of inflammatory cells were evaluated to investigate the function of abrocitinib on the 1st day post-injury. Furthermore, the JAK1/signal transducer and activator of transcription1 (STAT1)/nuclear factor kappa (NF-κB) pathway was assessed. Results: In vivo, abrocitinib treatment was found to shrink the trauma lesions. Compared to the TBI group, the abrocitinib treatment group showed better neurological function, less blood-brain barrier (BBB) leakage, improved intracranial blood flow, relieved inflammatory cell infiltration, and reduced levels of inflammatory cytokines. In vitro, abrocitinib treatment was shown to reduce the pro-inflammatory M1 microglia phenotype and shift microglial polarization toward the anti-inflammatory M2 phenotype. The WB and IHC results showed that abrocitinib played a neuroprotective role by restraining JAK1/STAT1/NF-κB levels after TBI. Conclusions: Collectively, abrocitinib treatment after TBI is accompanied by improvements in neurological function consistent with radiological, histopathological, and biochemical changes. Therefore, abrocitinib can indeed reduce excessive neuroinflammation by restraining the JAK1/STAT1/NF-κB pathway.Keywords:TBI;abrocitinib;neuroinflammation;JAK1/STAT1/NF-κB
研究领域:
神经科学
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药理学
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炎症
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创伤
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DOI
PubMed
高影响因子
MUSCLE & NERVE
·
2025
·Vol. 71
·期 3
·474-486
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IF 3.1
Zhuajin Bi,Qing Zhang,Huajie Gao,Huizhen Ge,Jiayang Zhan,Mengge Yang,Bitao Bu
Introduction/Aims Tofacitinib, a first-generation Janus kinase (JAK) 1/3 inhibitor, is commonly used for treating ulcerative colitis and rheumatoid arthritis. However, its role in myasthenia gravis (MG) remains unclear. This study aimed to evaluate the immunomodulatory effects of tofacitinib on experimental autoimmune myasthenia gravis (EAMG) and peripheral blood mononuclear cells (PBMCs) from patients with MG. Methods Flow cytometry, enzyme-linked immunosorbent assay (ELISA), quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blot were used to evaluate the effects of tofacitinib on T helper (Th) cell profiles, humoral immune responses, and the JAK-signal transducer and activator of transcription (STAT) pathway proteins. Results In vivo, tofacitinib significantly ameliorated EAMG severity in rats, reducing the proportions of Th1, Th17 and memory B cells, and anti-acetylcholine receptor (AChR) antibodies levels, while increasing the proportions of regulatory T (Treg) cells. In vitro, tofacitinib administration resulted in a significant decrease in the proportions of Th1 and IgG-secreting B cell, and a significant upregulation of Treg cells in mononuclear cells (MNCs) from EAMG rats, which was consistent with findings in PBMCs from MG patients. Further analysis revealed that tofacitinib inhibited CD4 + T cell differentiation into Th1 by decreasing phosphorylated STAT1 levels, while promoting Treg differentiation via increased phosphorylated STAT5 levels in MNCs from EAMG rats. Discussion Tofacitinib modulates Th cell profiles and humoral immune responses by targeting the JAK–STAT pathway, suggesting its potential as a therapeutic candidate for MG. Further clinical studies are warranted to evaluate the efficacy and safety of tofacitinib in MG patients.
研究领域:
免疫学
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药理学
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神经病学
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产品关联
DOI
PubMed
高影响因子
STEM CELLS
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2023
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IF 5.2
Li Zhi-hui,Chen Jun-feng,Zhang Jing,Lei Zi-ying,Wu Li-li,Meng Shi-bo,Wang Jia-lei,Xiong Jing,Lin Deng-na,Wang Jun-yi,Gao Zhi-liang,Lin Bing-liang
Acute-on-chronic liver failure (ACLF) is a severe disease with a high mortality. Macrophage-related inflammation plays a crucial role in ACLF development. Mesenchymal stem cells (MSCs) treatment was demonstrated to be beneficial in ACLF in our previous study; however, the underlying mechanisms remain unknown. Therefore, mouse bone marrow-derived MSCs were used to treat an ACLF mouse model or cocultured with RAW264.7/J774A.1 macrophages that were stimulated with LPS. Histological and serological parameters and survival were analyzed to evaluate efficacy. We detected changes of Mer tyrosine kinase (Mertk), JAK1/STAT6, inflammatory cytokines, and markers of macrophage polarization in vitro and in vivo. In ACLF mice, MSCs improved liver function and 48-h survival of ACLF mice and alleviated inflammatory injury by promoting M2 macrophage polarization and elevated Mertk expression levels in macrophages. This is significant, as Mertk regulates M2 macrophage polarization via the JAK1/STAT6 signaling pathway.
研究领域:
肝病学
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免疫学
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干细胞生物学
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细胞信号传导
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产品关联
DOI
PubMed
高影响因子
Arabian Journal of Chemistry
·
2024
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IF 5.3
Yi Chen,Shasha Song,Yongfang Wang,Xiaoli Zhang,Jiafen Zhang,Lili Wu,Jianbing Wu,Xinyu Li
Psoriasis is a common chronic inflammatory skin disease, which has seriously affected human health. Berberine is a plant alkaloid with significant anti-inflammatory effect. In this study, we aimed to determine whether topical application of berberine could ameliorate skin inflammation in psoriasis and explore the potential molecular mechanism. Imiquimod (IMQ)-induced psoriasis-like dermatitis in mice was firstly used to reveal the potential pathogenic mechanism. The transcriptome analysis showed that Janus kinase (JAK)-Signal transducer and activator of transcription (STAT) signaling pathway was significantly enriched in IMQ-induced dermatitis, which included the key genes such as Janus kinase 1 (JAK1), Interleukin-2 (IL2), Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA), Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit beta isoform (PIK3CB) and Signal transducer and activator of transcription 1 (STAT1). Network pharmacology and molecular docking then predicted that topical berberine may treat psoriasis by JAK-STAT signaling pathway, especially act on JAK1, IL2, PIK3CA and PIK3CB. Experimental studies in vivo further demonstrated that topical application of berberine could ameliorate IMQ-induced psoriasis-like skin inflammation by suppressing JAK-STAT signaling pathway. In addition, experimental studies in vitro showed that berberine could directly act on and enter into human immortalized keratinocytes (HaCaT cells). Meanwhile, berberine may inhibit the hyperproliferation and proinflammatory functions of HaCaT cells induced by Interferon-gamma (IFN-γ) via suppressing JAK1/STAT1 signaling pathway. In conclusion, this study suggested that berberine may be a promising topical agent to ameliorate skin inflammation in psoriasis.
研究领域:
皮肤病学
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药理学
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分子生物学
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免疫学
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产品关联
DOI
高影响因子
Scientific Reports
·
2015
·Vol. 5
·期 1
·1-17
·
IF 5.578
Cao Wei,Liu Ying,Zhang Ran,Zhang Bo,Wang Teng,Zhu Xianbing,Mei Lin,Chen Hongbo,Zhang Hongling,Ming Pinghong,Huang Laiqiang
Tyrosine kinase inhibitors (TKIs) are mostly used in non-small cell lung cancer (NSCLC) treatment. Unfortunately, treatment with Gefitinib for a period of time will result in drug resistance and cause treatment failure in clinic. Therefore, exploring novel compounds to overcome this resistance is urgently required. Here we investigated the antitumor effect of homoharringtonine (HHT), a natural compound extracted from Cephalotaxus harringtonia , on Gefitinib-resistant NSCLC cell lines in vitro and in viv o. NCI-H1975 cells with EGFR T790M mutation are more sensitive to HHT treatment compared with that of A549 cells with wild type EGFR. HHT inhibited cells growth, cell viability and colony formation, as well as induced cell apoptosis through mitochondria pathway. Furthermore, we explored the mechanism of HHT inhibition on NSCLC cells. Higher level of interleukin-6 (IL-6) existed in lung cancer patients and mutant EGFR and TGFβ signal requires the upregulation of IL-6 through the gp130/JAK pathway to overactive STAT3, an oncogenic protein which has been considered as a potential target for cancer therapy. HHT reversiblely inhibited IL-6-induced STAT3 Tyrosine 705 phosphorylation and reduced anti-apoptotic proteins expression. Gefitinib-resistant NSCLC xenograft tests also confirmed the antitumor effect of HHT in vivo . Consequently, HHT has the potential in Gefitinib-resistant NSCLC treatment.
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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细胞生物学
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DOI
PubMed
高影响因子
Food Bioscience
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2023
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IF 5.2
Yanping Fan,Meilan Xue,Tianhu Shan,Yixian Bai,Huaqi Zhang,Man Liu,Peng Wang,Xi Liang,Hui Liang
Alcoholic liver fibrosis (ALF) is a reversible pathological change in the liver caused by chronic alcohol consumption and is associated with the activation of hepatic stellate cells . Recent findings suggest that niacin can lower triglyceride levels and exert potent antioxidant effects in liver damage. However, the therapeutic effects and molecular mechanisms of niacin in liver fibrosis remain unclear. Therefore, this study aimed to investigate the effects and mechanisms of niacin in ALF using in vivo and in vitro experiments. To establish a murine model of ALF, male C57BL/6N mice were fed a Lieber–DeCarli liquid diet containing 4 % (vol/vol) ethanol and injected with carbon tetrachloride twice weekly (2 mL/kg) for 8 weeks. L-02 and LX2 cells were treated with 400 μM acetaldehyde for 24 h to establish an in vitro ALF model. Serum parameters were examined to investigate the protective effects of niacin against ALF, and network pharmacology was used to identify potential targets and pathways of niacin. Niacin protects against ALF by suppressing the serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase , and alkaline phosphatase . Additionally, niacin treatment ameliorated liver fibrosis by improving the antioxidant system, inhibiting heat shock protein 90 (HSP90) activation, promoting signal transducer and activator of transcription 3 (STAT3) ubiquitination , and suppressing the JAK1/STAT3 signaling pathway . Collectively, this study provides experimental evidence that niacin protects against ALF by downregulating the HSP90/JAK1/STAT3 signaling pathway.
研究领域:
药理学
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肝病学
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分子生物学
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细胞生物学
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产品关联
DOI
高影响因子
MOLECULAR MEDICINE
·
2024
·Vol. 30
·期 1
·1-15
·
IF 6
Zhang FengQi,Zhang YiYang,Zhou JiaWang,Cai Ying,Li ZhiYu,Sun Jing,Xie ZhiJun,Hao GuiFeng
Background Rheumatoid arthritis, a chronic autoimmune disease, is characterized by synovial hyperplasia and cartilage erosion. Here, we investigated the potential mechanism of action of quercetin, the main component of flavonoids, in treating rheumatoid arthritis. Object To examine the anti-arthritic effects of quercetin and elucidate the specific mechanisms that differentiate its metabolic effects on autoimmune and inflammatory responses at the synovial cell level. Methods We created a collagen-induced arthritis (CIA) model in Wistar rats, which were administered quercetin (50 or 100 mg/kg) continuously for four weeks via stomach perfusion. The arthritis score, histopathological staining, radiological assessment, and serum biochemical parameters were used to study the impact of quercetin on disease improvement. Additionally, immunofluorescence was employed to detect JAK1/STAT3/HIF-1α expression in rat joints. Moreover, the effects of quercetin (20, 40, and 80 µmol/L) on the properties and behavior of synovial fibroblasts were evaluated in an in vitro MH7A cell model using flow cytometry, CCK8, and transwell assays. Further, the mRNA expression levels of inflammatory cytokines IL1β, IL6, IL17, and TNFα were assessed by quantitative real-time PCR. Glucose, lactate, lactate dehydrogenase, pyruvate, pyruvate dehydrogenase, and adenosine triphosphate assay kits were employed to measure the metabolic effects of quercetin on synovial fibroblasts. Finally, immunoblotting was used to examine the impact of quercetin on the JAK1/STAT3/HIF-1α signaling pathway in synovial fibroblasts. Results In vivo experiments confirmed the favorable effects of quercetin in CIA rats, including an improved arthritis score and reduced ankle bone destruction, in addition to a decrease in the pro-inflammatory cytokines IL-1β, IL-6, IL-17, and TNF-α in serum. Immunofluorescence verified that quercetin may ameliorate joint injury in rats with CIA by inhibiting JAK1/STAT3/HIF-1α signaling. Various in vitro experiments demonstrated that quercetin effectively inhibits IL-6-induced proliferation of MH7A cells and reduces their migratory and invasive behavior, while inducing apoptosis and reducing the expression of the pro-inflammatory cytokines IL1β, IL6, IL17, and TNFα at the mRNA level. Quercetin caused inhibition of glucose, lactate, lactate dehydrogenase, pyruvate, and adenosine triphosphate and increased pyruvate dehydrogenase expression in MH7A cells. It was further confirmed that quercetin may inhibit energy metabolism and inflammatory factor secretion in MH7A cells through JAK1/STAT3/HIF-1α signaling. Conclusions Quercetin’s action on multiple target molecules and pathways makes it a promising treatment for cartilage injury in rheumatoid arthritis. By reducing joint inflammation, improving joint metabolic homeostasis, and decreasing immune system activation energy, quercetin inhibits the JAK1/STAT3/HIF-1α signaling pathway to improve disease status.
研究领域:
免疫学
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药理学
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风湿病学
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分子生物学
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DOI
PubMed
高影响因子
FEBS Journal
·
2021
·Vol. 289
·期 7
·1968-1983
·
IF 5.542
Ting-Ting Wei,Meng-Yuan Zhang,Xin-Hua Zheng,Tian-Hua Xie,Wenjuan Wang,Jian Zou,Yan Li,Hong-Ying Li,Jiping Cai,Xiaolu Wang,Jianxin Tan,Xusheng Yang,Yong Yao,Lingpeng Zhu
Retinal pigment epithelium (RPE) cell damage is implicated in the pathogenesis of age-related macular degeneration (AMD). An increase of interferon-γ (IFN-γ) levels was observed in patients with AMD, but whether inflammatory factors are causally related to AMD progression is unclear. Here, we demonstrate a direct causal relationship between IFN-γ and RPE cell death. IFN-γ induced human retinal pigment epithelial cell (ARPE-19) death accompanied by increases in Fe 2+ , reactive oxygen species, lipid peroxidation, and glutathione (GSH) depletion, which are main characteristics of ferroptosis. Mechanistically, IFN-γ upregulates the level of intracellular Fe 2+ through inhibiting Fe 2+ efflux protein SLC40A1 and induces GSH depletion by blocking cystine/glutamate antiporter, System xc-. At the same time, treatment with IFN-γ decreases the level of glutathione peroxidase 4 (GPx4), rendering the cells more sensitive to ferroptosis. JAK1/2 and STAT1 inhibitors could reverse the reduction of SLC7A11, GPx4 and GSH expression induced by IFN-γ, indicating IFN-γ induces ARPE-19 cell ferroptosis via activation of the JAK1-2/STAT1/SLC7A11 signaling pathway. The above results were largely confirmed in IFN-γ-treated mice in vivo . Finally, we used sodium iodate (NaIO 3 )-induced retinal degeneration to further explore the role of ferroptosis in AMD in vivo . Consistent with the role of IFN-γ, treatment with NaIO 3 decreased SLC7A11, GPx4 and SLC40A1 expressions. NaIO 3 -induced RPE damage was accompanied by increased iron, lipid peroxidation products (4-hydroxynonenal, malondialdehyde), and GSH depletion, and ferroptosis inhibitors could reverse the above phenomenon. Taken together, our findings suggest that inhibiting ferroptosis or reducing IFN-γ may serve as a promising target for AMD.
研究领域:
眼科学
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细胞生物学
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分子生物学
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病理学
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产品关联
DOI
PubMed
高影响因子
American Journal of Translational Research
·
2019
·
IF 3.266
Hua Liu,Xiao-De Feng,Beng Yang,Rong-Liang Tong,Yue-Jie Lu,Di-Yu Chen,Lin Zhou,Hai-Yang Xie,Shu-Sen Zheng,Jian Wu
Dimethyl fumarate (DMF) is generally used to treat psoriasis and multiple sclerosis. In the present study, we aimed to investigate the effects of DMF on hepatocellular carcinoma progression and its mechanism of action. In vitro , cell viability was examined using CCK-8 assay; cell cycle was analyzed by flow cytometry; angiogenesis was detected using tube formation assay; and autophagic flux assay results were examined using fluorescence microscopy. We also used western blotting to explore the potential mechanisms. In vivo , tumor xenograft experiment was performed with nude mice, and liver function, renal function, and routine blood counts were assessed using biochemical tests. Dimethyl fumarate inhibited tumor growth and angiogenesis in hepatocellular carcinoma, both in vitro and in vivo . Dimethyl fumarate decreased autophagy in hepatocellular carcinoma cells. Treatment with DMF activated SOCS3, which led to repression of JAK1 and STAT3 phosphorylation. DMF inhibited cell proliferation, angiogenesis, and autophagy via activation of the SOCS3/JAK1/STAT3 signaling pathway. This finding may provide a novel approach for the treatment of hepatocellular carcinoma.
研究领域:
肿瘤学
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分子生物学
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药理学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Si-yu Liu,Chang-qing Wang,Tong-tong Luo,Gui-juan Cui,Yuan Zhang,Xing-ju Zou,Zi-jian Zhang,Wen-xiu Liu,Chen Sun,Cheng Peng
Ethnopharmacological relevance Scutellaria baicalensis , a traditional Chinese medicine herb, has been classically used to treat diarrhea and dysentery caused by damp heat in Traditional Chinese Medicine. And it has been demonstrated to alleviate colonic mucosal inflammation in ulcerative colitis. However, the mechanism through which its main active ingredient, baicalin, alleviates ulcerative colitis remains unclear. Aim of the study This study investigated whether baicalin regulates macrophages to ameliorate ulcerative colitis through the JAK1/STAT1/SOCS1 pathway. Materials and methods LPS-induced RAW264.7 cells were used to investigate the anti-inflammatory and regulatory effects of baicalin on macrophage polarization. The NO content was assessed by a Griess assay, and label-free optical diffraction tomography for live-cell imaging and confocal imaging were conducted to observe macrophage polarization and analyze the expression of CD86 and CD206. The protective effect of baicalin on DSS-induced colitis mice was evaluated through the Disease Activity Index (DAI) system, endoscopy, enzyme-linked immunosorbent assay (ELISA), hematoxylin and eosin (HE) staining, Alcian Blue periodic acid Schiff (AB-PAS) staining, and immunofluorescence. Macrophages in the lamina propria of the colon were analyzed by tiling light sheet microscopy imaging and flow cytometry. Western blotting (WB) was used to evaluate the expression of JAK1/STAT1/SOCS1 pathway members, and the expression of the downstream transcription factors were quantified through qPCR. Key results Baicalin markedly inhibited NO levels induced by LPS and delayed the timing and quantity of macrophage polarization toward the M1 phenotype. Furthermore, baicalin ameliorated the symptoms of colitis in mice, such as diarrhea, hematochezia, weight loss, colon shortening, decreased spleen weight, pathological changes, intestinal mucosal barrier dysfunction, and decreased DAI and inflammatory factor levels. Moreover, baicalin promoted macrophage polarization toward the M2 phenotype and inhibited the polarization of M1 macrophages in the intestinal lamina propria. Mechanistically, baicalin inhibited the phosphorylation of JAK1 and STAT1 and restored the negative feedback inhibition of JAK1/STAT1 by upregulating SOCS1. In addition, baicalin reduced the mRNA levels of downstream genes. Conclusions and implications Baicalin can alleviate intestinal inflammation, ameliorate intestinal barrier damage, and regulate macrophage polarization by inhibiting M1 macrophage polarization in an ulcerative colitis model. This protective effect was achieved through the JAK1/STAT1/SOCS1 pathway.
研究领域:
药理学
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免疫学
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民族药理学
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分子生物学
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胃肠病学
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产品关联
DOI
PubMed
高影响因子
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