KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
·
2025
·Vol. 29
·期 4
·487
·
IF 2.2
Tingting Yu,Zirui Yuan,Jiaona Yu,Lu Chen,Wei Hao,Xiaohui Xu
Melittin (MEL) is the main bioactive component of bee venom and has been reported to have various pharmacological effects. This study investigates the protective effect of MEL on MPP + -injured HT22 cells and the possible mechanisms involved. We treated the cells with 4 mM MPP + for 24 h to induce a cellular injury model. HT22 cells were pretreated with 0.1 µM MEL for 6 h and then exposed to 4 mM MPP + for 24 h. We measured cell viability, the expression of Bax, the indicators and protein levels associated with apoptosis and parthanatos, and the co-localisation of MEL and mitochondria, and mitochondrial function-related indices such as the mitochondrial membrane potential (MMP) and mito-SOX. We show that PAR protein expression was significantly increased in the MPP + -treated cell model and that the parthanatos inhibitor DPQ significantly reduced MPP + -induced cell death, suggesting that MPP + can cause PARP1-dependent cell death. MEL significantly inhibited cell death, increased cell viability as well as NAD+ and ATP levels, increased the expression of Bcl-2 and suppressed the activation of Bax, cleaved-caspase3, and cleaved-PARP1. Moreover, MEL was found to be localised on the mitochondria of HT22 cells and to improve mitochondrial functions including increased MMP and decreased mitochondrial reactive oxygen species. We speculate that MEL may protect neurons against MPP + -induced HT22 cell injury by inhibiting Bax activation, suppressing changes in mitochondrial permeability, and improving mitochondrial function, thereby preventing cell parthanatos and apoptosis.
研究领域:
神经生物学
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药理学
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细胞生物学
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DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
·
2018
·
IF 3.457
Xiang-Feng Guo,Ji-Peng Liu,Si-Quan Ma,Peng Zhang,Wen-De Sun
5-Fluorouracil (5-Fu) and cisplatin (DDP) as important therapies in treatment of human gastric cancer have been widely determined. However, the therapeutic effects are usually hampered due to drug resistance or toxicity at high concentrations for application. Avicularin (AL, quercetin-3-α- l -arabinofuranoside), a bio-active flavonol isolated from a number of plants, has been reported to display diverse pharmacological properties. In this study, we explored the hypothesis by which AL reversed 5-Fu or DDP resistance in gastric cancer and the underlying molecular mechanism. Here, in vitro, the drug-resistant cancer cells were incubated to AL or DDP alone or the combination of AL and DDP. Then, MTT, colony formation, Hoechst 33258 , flow cytometry and western blot analysis were used to investigate the effects of AL in the regulation of drug-resistance gastric cancer cells. The results indicated that AL treatment markedly re-sensitizes the drug resistant cells (SGC-7901/5-Fu and SGC-7901/DDP) to cytotoxicity of 5-Fu or DDP. Molecular mechanism analysis indicated that AL and DDP combination treatment enhanced apoptosis in SGC-7901/DDP cells, accompanied with the up-regulation of cleaved Caspase-3 and PARP, as well as the activation of pro-apoptotic signals, including Bax and BOK. Significantly, down regulation of Bax or BOK expressions using Bax siRNA or BOK siRNA decreased the inhibitory role of DDP in apoptosis of SGC-7901/DDP cells pretreated with AL, demonstrating that AL-reversed DDP resistance was associated with Bax and BOK expression. In vivo, AL and DDP combination significantly reduced gastric tumor growth. Immunohistochemical analysis indicated that co-treatment of AL and DDP significantly induced apoptosis, and reduced tumor cell proliferation in tumor tissue samples. Furthermore, we also found that the Bax, BOK, cleaved Caspase-3 and PARP expression in tumor tissues were highly induced by AL and DDP co-treatment. Together, our findings may provide a novel combination therapeutic strategy in treatment of human gastric cancer.
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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癌症治疗
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DOI
PubMed
高影响因子
EXPERIMENTAL NEUROLOGY
·
2025
·
IF 4.2
Jun Fu,Chengjie Ding,Wenqing Li,Jiali Lei,He Wang,Lingfei Meng,Xiaoya Lin,Weiyuan Chen,Hongchang Gao
Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, with hallmark pathological features including Aβ deposition and tau protein hyperphosphorylation. These pathological alterations are particularly prominent in the Prefrontal Cortex (PFC) and exert profound effects on cognitive function. The present study aimed to reveal key proteins in the PFC and provide insight into their potential mechanisms of action in AD. Accordingly, proteomic analysis was conducted to profile differential proteins in 5 × FAD mice, followed by in vivo and in vitro validation of core proteins through AAV-mediated interference of target gene expression. Furthermore, transcriptomics and molecular biology techniques were employed to confirm the underlying mechanisms of action of core proteins in AD. The results demonstrated that ELAVL1 was significantly upregulated in the PFC of AD mice. Behavioral experiments revealed that inhibition of ELAVL1 expression markedly improved long-term memory in AD mice. Immunostaining and Western blot analyses confirmed that suppressing ELAVL1 expression alleviated Aβ1–42 deposition and apoptosis. In vitro experiments indicated that knocking down ELAVL1 significantly reduced the apoptotic response of SH-SY5Y cells induced by Aβ1–42 and APP/Swe cells. Transcriptomic analysis further revealed that ELAVL1 regulates Aβ1–42-induced apoptosis via activation of the Bcl-2/Bax pathway. Notably, immunofluorescence co-localization staining and pull-down assays confirmed that ELAVL1 directly interacts with APP. Collectively, these findings provide valuable insights into the molecular mechanisms underlying AD and suggest ELAVL1 as a promising therapeutic target for AD.
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DOI
PubMed
高影响因子
JOURNAL OF APPLIED TOXICOLOGY
·
2020
·Vol. 40
·期 11
·1526-1533
·
IF 2.997
Yalei Yu,Youyou Zhang,Jie Zhang,Chuhuai Guan,Liang Liu,Liang Ren
Cantharidin is of high medicinal value but has strong toxicity. Nowadays, multiple research has focused on the mechanism of its antitumor activity while research on toxicological profiles associated with cantharidin poisoning is still limited. Its hepatotoxicity has attracted attention recently for the crucial role of the liver in detoxification. Here, we aim to find a potential mechanism for cantharidin-induced acute hepatotoxicity with a view to assisting subsequent research or clinical use or detoxification. Twenty-one male Sprague-Dawley rats were randomly divided into control, low-dose (1.34 mg/kg) and high-dose (2.67 mg/kg) cantharidin exposure groups. We used hematoxylin-eosin to observe pathological changes and used immunofluorescent staining, western blotting and real-time quantitative polymerase chain reaction to detect the expression of the markers. The main pathological changes in livers of cantharidin-treated rats were necrosis, inflammatory infiltration and hemorrhage. We found coexpression of tumor necrosis factor alpha (TNF-α), IkappaB kinase-alpha (IKK-α) and caspase3 by immunofluorescent staining in livers of cantharidin-treated rats. Compared with the control, the levels of TNF-α, IKK-α and caspase3 increased significantly in the experimental groups ( P < .05). The ratio of B-cell lymphoma-2 (Bcl-2)/Bax increased in the low-dose group but decreased in the high-dose group ( P < .05). Cantharidin exposure raised IKK-α mRNA and caspase3 mRNA levels ( P < .05). In conclusion, the participation of TNF-α, IKK-α, Bcl-2, Bax and caspase3 uncovered a novel mechanism underlying cantharidin-induced acute hepatotoxicity, and the mechanism needs to be studied further.
研究领域:
药理学
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毒理学
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分子生物学
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DOI
PubMed
高影响因子
BIOLOGICAL & PHARMACEUTICAL BULLETIN
·
2020
·
IF 1.863
Yuanguo Xiong,Hao Lu,Hanlin Xu
Hepatic fibrosis (HF) is a common disease, with currently no available treatment. Galangin, a natural flavonoid extracted from Alpinia officinaruim Hance, has multiple effects demonstrated in previous studies. The aim of the present study was to explore the anti-fibrogenic effect of galangin in vitro, and research its potential molecular mechanisms. LX-2 cells were chosen as an in vitro HF model, and were treated with galangin in different concentrations. Cell viability was analyzed using Cell Counting Kit-8 (CCK-8) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, cell apoptosis was measured using flow cytometry, and the anti-fibrogenic effect of galangin was determined using quantitative reverse transcription polymerase chain reaction (RT-qPCR), immunofluorescence, and western blotting. The results show that the proliferation of LX-2 cells was efficiently inhibited by galangin, and apoptosis was induced in a dose-dependent manner. Both the mRNA and protein expression of α-SMA and collagen I were markedly downregulated. Galangin also inhibited the PI3K/Akt and Wnt/β-catenin signaling pathways and increased the Bax/Bcl-2 ratio. The results of this study suggest that galangin has an anti-fibrogenic effect and may represent a promising agent in the treatment of hepatic fibrosis.
研究领域:
药理学
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细胞生物学
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分子生物学
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肝病学
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DOI
PubMed
高影响因子
EXPERIMENTAL PHYSIOLOGY
·
2021
·Vol. 106
·期 4
·983-993
·
IF 2.969
Changfeng Shan,Ronghua Wang,Shuai Wang,Zongmeng Zhang,Chaofeng Xing,Wenbin Feng,Zhenggang Zhao,Sujin Zhou,Allan Zijian Zhao,Yunping Mu,Fanghong Li
New Findings What is the central question of this study? What is the protective benefit of n −3 polyunsaturated fatty acids (PUFAs) on liver fibrosis and what are the relevant signalling pathways in a transgenic mouse model overexpressing the mfat-1 enzyme? What is the main finding and its importance? n −3 PUFA elevation strongly prevented carbon tetrachloride (CCl 4 )-induced hepatic damage and inhibited the activation of hepatic stellate cells. n −3 PUFAs suppressed CCl 4 -induced activation of mTOR, elevated Bcl-2 expression, and reduced Bax level, suggesting that n −3 PUFAs can render strong protective effects against liver fibrosis and point to the potential of mfat-1 gene therapy as a treatment modality. Liver fibrosis is a reversible wound healing response with excessive accumulation of extracellular matrix proteins. It is a globally prevalent disease with ultimately severe pathological consequences. However, very few current clinical therapeutic options are available. Nutritional addition of n −3 polyunsaturated fatty acids (PUFAs) can delay and lessen the development of liver fibrosis. Herein, this study examined the protective benefit of n −3 PUFAs on liver fibrosis and the relevant signalling pathways using a transgenic mouse model overexpressing the mfat-1 enzyme that converts n −6 to n −3 PUFAs. Male C57BL/6 wild-type and mfat-1 transgenic mice were administered carbon tetrachloride (CCl 4 ) or control corn oil by intraperitoneal injection. Blood alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were subsequently measured. CCl 4 -induced hepatic damage and fibrosis were assessed using haematoxylin–eosin and Masson's trichrome staining. Western blot assays were used to detect and quantify fibrosis-related proteins and mechanistic target of rapamycin (mTOR) and B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) signalling components. The direct effect of docosahexaenoic acid (DHA) on primary hepatic stellate cells (HSCs) was also investigated in a co-culture experiment. n −3 PUFAs, as a result of mfat-1 activity, had a strong protective effect on liver fibrosis. The elevation of ALT and AST induced by CCl 4 was significantly lessened in the mfat-1 mice. Histological determination revealed the protective effects of n −3 PUFAs on liver inflammation and collagen deposition. Co-incubation with DHA reduced the expression of profibrogenic factors in the primary HSCs. Moreover, mfat-1 transgenic mice showed significant reduction of proteins that are involved in mTOR and Bcl-2/Bax signalling pathways. Collectively, these results suggest that n −3 PUFA elevation strongly prevents CCl 4 -induced hepatic damage by directly inhibiting the activation of HSCs and regulating the basal activity of the mTOR and Bcl-2/Bax signalling pathways. Gene therapy applying mfat-1 and elevating n −3 PUFAs represents a promising treatment strategy to prevent liver fibrosis.
研究领域:
肝病学
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分子生物学
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药理学
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营养学
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DOI
PubMed
高影响因子
JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
·
2023
·
IF 4.4
Wenyuan Zhang,Songjuan Zhuang,Hui Guan,Feng Li,Hui Zou,Dapeng Li
Excessive apoptosis can kill normal cells and lead to liver damage, heart failure and neurodegenerative diseases. Polyphenols are secondary metabolites of plants that can interact with proteins to inhibit toxins and disease-related apoptosis. Bax is the major pro-apoptotic protein that disrupts the outer mitochondrial membrane to induce apoptosis, but limited studies have focused on the interaction between polyphenols and Bax and the associated anti-apoptotic mechanisms, especially at the atomic level. In this article, we collected 69 common polyphenols for active ingredient screening targeting Bax. Polyphenols with better and worse molecular docking scores were selected, and their anti-apoptosis effects were compared using the H2O2-induced HepG2 cell model. The interactions between the selected polyphenols and Bax protein were analyzed using molecular dynamics simulation to explore the molecular mechanism underlying the anti-apoptosis effect. Secoisolariciresinol diglucoside (SDG) and Epigallocatechin-3-gallate (EGCG) with the best affinity for Bax (−6.76 and −6.52 kcal/mol) reduced the expression of cytochrome c and caspase 3, decreasing the apoptosis rate from 52 to 11% and 12%. Molecular dynamics simulation results showed that Bim unfolded the α1-α2 loop of Bax, and disrupted the non-bond interactions between the loop (Pro-43, Glu-44 and Leu-45) and surface (Ile-133, Arg-134 and Met-137) residues, with binding free energy changed from −15.0 to 0 kJ/mol. The hydrogen bonds and van der Waals interactions formed between polyphenols and Bax prevented the unfolding of the loop. Taken together, our results proved that polyphenols can inhibit apoptosis by maintaining the unactivated conformation of Bax to reduce outer mitochondrial membrane damage.Communicated by Ramaswamy H. Sarma
研究领域:
药理学
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分子生物学
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生物化学
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细胞生物学
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DOI
PubMed
高影响因子
Frontiers in Immunology
·
2022
·
IF 8.786
Liu Senyue,Luo Lin,Zuo Fengyuan,Geng Yi,Ou Yangping,Chen Defang,Yang Shiyong,Luo Wei,Wang Yan,Wang Jun,Huang Xiaoli
Myxobolus, a major harmful type of myxospora, is one of the main parasitic pathogens of freshwater fish. Once myxoboliosis occurs, treatment can be extremely difficult. Therefore, clear understandings of the etiology of myxoboliosis and its pathological mechanism are keys for prevention and control. Here, histology, transmission electron microscopy, transcriptome study, tunel assay, and immunohistochemistry were carried out, revealing the morphology, pathological effects as well as host response mechanism of goldfish gill to Myxobolus ampullicapsulatus. Histological studies showed that the mature spores of Myxobolus ampullicapsulatus were composed of three parts, the spore shell, sporoplasm and bottle shaped polar capsule containing double S-shaped polar filaments. Transcriptome analysis revealed that Myxobolus ampullicapsulatus -infected (Myx) goldfish gills were characterized by apoptosis activation mediated by “p53 signaling pathway” with significantly up-regulated apoptosis-related differential genes dominated by p53-Bcl2/Bax signaling pathway. In addition, tunel assay revealed severe gill apoptosis in the Myx group. Transcriptome analysis also revealed that Myx group showed changes in immune response and significantly down-regulated immune-related differential genes. Beyond that, immunohistochemistry showed that there was no significant increase in the number of gill lymphocyte after parasite infection. These results suggest that the pathological mechanism of Myxobolus ampullicapsulatus infection on gills of goldfish may be related to apoptosis and immunosuppression. Subsequent qRT-PCR showed that apoptosis-related genes (Caspase3,Bad, Bax) and anti-inflammatory gene IL-10 were significantly increased, while immune-related pro-inflammatory genes (IL-1β, IL-8) were markedly down-regulated, further verifying the transcriptome results. Based on the above results, we concluded that p53-Bcl2/Bax related networks that dominant the expression of apoptosis genes were activated while immunity was suppressed in the gills of Myxobolus ampullicapsulatus infected goldfish. Our study is not only of benefit to enrich the taxonomy of Myxobolus but also clarifies its pathogenic mechanism, thus providing targets for prevention and control of myxoboliosis.
研究领域:
鱼类病理学
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分子生物学
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寄生虫学
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免疫学
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转录组学
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产品关联
DOI
PubMed
高影响因子
Molecular Medicine Reports
·
2016
·Vol. 14
·期 1
·904-910
·
IF 1.559
Liandi Xie,Yang Wu,Zongjing Fan,Yang Liu,Jixiang Zeng
In the present study, the mechanisms associated with the Astragalus polysaccharide (APS)-mediated protection of human cardiac microvascular endothelial cells (HCMEC) against hypoxia/reoxygenation (HR) injury were investigated. Pretreatment of HCMECs with APS at various concentrations was performed prior to Na2S2O4-induced HR injury. Subsequently, cell viability and apoptosis were measured by MTT and Hoechst assays, respectively. The viability of HCMECs was reduced by Na2S2O4 and apoptosis was enhanced; however, cell viability was observed to be increased by APS via inhibition of apoptosis. Additionally, intracellular reactive oxygen species (ROS), Ca2+, nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT), B‑cell lymphoma‑2 (Bcl‑2), Bcl‑2 associated X protein (Bax) and caspase‑3 were measured using detection kits or western blot analysis. In HCMECs with HR injury, the levels of ROS and Ca2+, MDA and Bax expression levels, and the activity of caspase‑3 were elevated. By contrast, the level of NO, the protein expression levels of SOD, Bcl‑2 and PI3K, and the phosphorylation of AKT were decreased. However, compared with the HR group, the effects of HR injury were significantly reduced by APS, with APS providing a protective effect on HCMECs, particularly at higher doses. The current study concluded that APS protects HCMECs from Na2S2O4‑induced HR injury by reducing the levels of ROS, Ca2+, MDA and Bax, inhibiting the activity of caspase‑3, and enhancing the levels of NO, SOD, Bcl‑2, PI3K and phosphorylated AKT. These results may provide an insight into the clinical application of APS and novel therapeutic strategies for HR injury.
研究领域:
心血管研究
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分子生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
BRAIN RESEARCH BULLETIN
·
2022
·
IF 3.715
Xiaohui Xia,Shuai Wang,Lirong Wu,Guoxing Li,Kaiwen Hou,Anyong Yu,Zhao Yang
Background Intracerebral hemorrhage (ICH) is a serious disease with high mortality and morbidity, and effective treatment is limited. A large amount of evidence suggests that the inflammatory response contributes to secondary brain damage following ICH. TIPE2 is an essential negative regulator of both innate and adaptive immunity, and depletion of TIPE2 causes inflammatory disease. However, the possible role of TIPE2 following ICH has not been reported. Methods In this study, we investigated TIPE2 levels and inflammation in microglia treated with erythrocyte lysate in vitro. In addition, we analyzed the role of Bcl-2/Bax/cleaved caspase-3 apoptotic pathways in ICH mice. Furthermore, we observed proinflammatory cytokine production, BBB disruption, cerebral water content and neurological damage in ICH mice. Results We found that TIPE2 levels were significantly decreased in erythrocyte lysate-treated microglia compared to control microglia.Upregulation of TIPE2 decreased microglia activation and cytokine production and accelerated brain damage in ICH mice. Furthermore, upregulation of TIPE2 decreased the higher ratio of Blc-2/Bax and increased cleaved caspase-3 levels in ICH mice. In addition, upregulation of TIPE2 attenuated proinflammatory cytokine production, BBB disruption, and severe brain inflammation after ICH. Conclusion These results demonstrated that TIPE2 was negatively correlated with the pathogenesis of ICH, which prevented brain injury and attenuated deleterious inflammatory responses following ICH. TIPE2 might serve as a novel target for ICH therapy.
研究领域:
神经科学
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分子生物学
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病理学
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药理学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2024
·
IF 7.7
Shaojie Zhang,Renjie Gao,Baocong Ding,Junhao Li,Tanggan Wang,Jiaheng Chen,Chong Li,Yukun Jiao,Lijun Song
Combining selenium nanoparticles (SeNPs) with bioactive polysaccharides is one of the effective ways to overcome the shortcomings of SeNPs and polysaccharide and obtain novel antitumor drug candidates. In this study, a heteropolysaccharide (MTP70) with moderate antihepatoma activity was isolated from the stems of Marsdenia tenacissima (Roxb.) Wight et Arn. To further improve the antihepatoma activity of MTP70 and the application of SeNPs, a novel stable nanoparticle (MTP-SeNP) was designed and fabricated. MTP-SeNPs (Se content of 8.25 %) were characterized as monodisperse spherical nanoparticles (50 nm) with MTP70 wrapped on the surface of the SeNPs by the formation of C O⋯Se bonds and possessed high stability and good dispersion in water for almost a month. In addition, MTP-SeNPs showed higher inhibitory effect compared with MTP70. MTP-SeNPs could effectively inhibit the proliferation, invasion, and metastasis of HePG2 cells by inducing apoptosis and arresting the cell cycle at the S phase, which were closely related to the activation of the Bax/Bcl-2/Caspases and p-21/Akt/Cyclin A2 signaling pathways. Our results provide a theoretical basis for further development and application of M. tenacissima polysaccharide, and show that MTP-SeNPs could be explored as a promising anti-hepatoma agent in the pharmaceutical and biomedical industries.
研究领域:
药理学
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纳米技术
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肿瘤学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Yinhuang Gao,Ke Ma,Zhibo Zhu,Yan Zhang,Qiong Zhou,Jing Wang,Xiaowen Guo,Liuting Luo,Haitao Wang,Kang Peng,Menghua Liu
Background Vascular dementia (VaD) is one of the most common clinical syndromes of progressive neurocognitive dysfunction with uncertain mechanisms. Modified Erchen decoction (MECD), developed from “Erchen decoction (ECD)” recorded in “Taiping Huimin Heji Jufang”, showed a good effect in the treatment of VaD. However, its therapeutic mechanism is still unclear. Purpose This study aimed to elucidate the multi-target mechanisms of MECD against VaD in vivo and in vitro . Methods VaD model was established by two-vessel obstruction (2-VO) in Sprague-Dawley rats. Six groups, including the control, 2-VO operation, MECD treatment (2.5, 5.0 and 10.0 g kg −1 d −1 ), donepezil hydrochloride (positive control, 0.45 g kg −1 d −1 ) were designed in the whole experiment. After oral administration for 4 weeks, the effects of MECD were verified by behavioral experiments, histological observation, and biochemical index analysis. The chemical profiling of MECD was performed by UHPLC-Orbitrap Fusion-HRMS, and a "compound-target-pathway" multivariate network was constructed to validate and elucidate its pharmacological mechanisms. Results Compared with 2-VO group, MECD treatment significantly alleviated anxiety and improved spatial memory in VaD rats according to the open field test (OFT) and Y-maze test. A significant increase in neuron number was observed from hematoxylin and eosin (H&E) stained images in cornu ammonis 1 (CA1) of the hippocampal region after MECD treatment. On the one hand, MECD reduced the plasma levels of triglyceride (TG), low-density lipoprotein (LDL), malondialdehyde (MDA), and amyloid-beta 42 (Aβ42), and inhibited mRNA expression of interleukin-1 beta ( Il-1β ) and Il-6 in the hippocampus. On the other hand, superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) were significantly increased after treatment with MECD. Moreover, MECD reduced the mRNA expression and protein expression of janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), c-Jun N-terminal kinase (JNK), and BCL2-associated X (BAX) in the brain of 2-VO rats. Furthermore, 71 compounds were identified from the extract of MECD. Among them, liquiritin and isochlorogenic acid C gave inhibiting effects on the mRNA expression of Jnk . In addition, liquiritin and hesperetin were conformed with the inhibition of Jak2 transcription level in vitro experiments. Conclusion MECD has demonstrated a significant amelioration effect on cognitive dysfunction in VaD rats via JAK2/STAT3 and JNK/BAX signaling pathways , which represents an innovative insight into the “activate blood and eliminate phlegm” theory.
研究领域:
药理学
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神经科学
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中医药
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分子生物学
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行为科学
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）