JOURNAL OF ETHNOPHARMACOLOGY
·
2023
·
IF 5.4
Xiao-Lu Jie,Zi-Rui Luo,Jin Yu,Zhe-Ren Tong,Qiao-Qiao Li,Jia-Hui Wu,Yi Tao,Pei-Shi Feng,Ji-Ping Lan,Ping Wang
Ethnopharmacological relevance Pi-Pa-Run-Fei-Tang (PPRFT) is an empirical TCM prescription for treating asthma. However, the underlying mechanisms of PPRFT in asthma treatment have yet to be elucidated. Recent advances have revealed that some natural components could ameliorate asthma injury by affecting host metabolism. Untargeted metabolomics can be used to better understand the biological mechanisms underlying asthma development and identify early biomarkers that can help advance treatment. Aim of the study The aim of this study was to verification the efficacy of PPRFT in the treatment of asthma and to preliminarily explore its mechanism. Materials and methods A mouse asthma model was built by OVA induction. Inflammatory cell in BALF was counted. The level of IL-6, IL-1β, and TNF-α in BALF were measured. The levels of IgE in the serum and EPO , NO , SOD , GSH-Px, and MDA in the lung tissue were measured. Furthermore, pathological damage to the lung tissues was detected to evaluate the protective effects of PPRFT. The serum metabolomic profiles of PPRFT in asthmatic mice were determined by GC-MS. The regulatory effects on mechanism pathways of PPRFT in asthmatic mice were explored via immunohistochemical staining and western blotting analysis. Results PPRFT displayed lung-protective effects through decreasing oxidative stress, airway inflammation , and lung tissue damage in OVA-induced mice, which was demonstrated by decreasing inflammatory cell levels, IL-6, IL-1β, and TNF-α levels in BALF, and IgE levels in serum, decreasing EPO, NO, and MDA levels in lung tissue, elevating SOD and GSH-Px levels in lung tissue and lung histopathological changes. In addition, PPRFT could regulate the imbalance in Th17/Treg cell ratios, suppress RORγt, and increase the expression of IL-10 and Foxp3 in the lung. Moreover, PPRFT treatment led to decreased expression of IL-6, p-JAK2/Jak2, p-STAT3/STAT3, IL-17, NF-κB, p-AKT/AKT, and p-PI3K/PI3K. Serum metabolomics analysis revealed that 35 metabolites were significantly different among different groups. Pathway enrichment analysis indicated that 31 pathways were involved. Moreover, correlation analysis and metabolic pathway analysis identified three key metabolic pathways: galactose metabolism; tricarboxylic acid cycle; and glycine, serine , and threonine metabolism. Conclusion This research indicated that PPRFT treatment not only attenuates the clinical symptoms of asthma but is also involved in regulating serum metabolism. The anti-asthmatic activity of PPRFT may be associated with the regulatory effects of IL-6/JAK2/STAT3/IL-17 and PI3K/AKT/NF-κB mechanistic pathways.
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2022
·Vol. 23
·期 18
·10887
·
IF 6.208
Jing Jie,Guomu Liu,Jingyue Feng,Desheng Huo,Yixuan Wu,Hongyan Yuan,Guixiang Tai,Weihua Ni
Our previous study found that CpG oligodeoxynucleotides 1826 (CpG 1826), combined with mucin 1 (MUC1)-maltose-binding protein (MBP) (M-M), had certain antitumor activity. However, this combination is less than ideal for tumor suppression (tumors vary in size and vary widely among individuals), with a drawback being that CpG 1826 is unstable. To solve these problems, here, we evaluate MF59/CpG 1826 as a compound adjuvant with M-M vaccine on immune response, tumor suppression and survival. The results showed that MF59 could promote the CpG 1826/M-M vaccine-induced tumor growth inhibition and a Th1-prone cellular immune response, as well as reduce the individual differences of tumor growth and prolonged prophylactic and therapeutic mouse survival. Further research showed that MF59 promotes the maturation of DCs stimulated by CpG1826/M-M, resulting in Th1 polarization. The possible mechanism is speculated to be that MF59 could significantly prolong the retention time of CpG 1826, or the combination of CpG 1826 and M-M, as well as downregulate IL-6/STAT3 involved in MF59 combined CpG 1826-induced dendritic cell maturation. This study clarifies the utility of MF59/CpG 1826 as a vaccine compound adjuvant, laying the theoretical basis for the development of a novel M-M vaccine.Keywords:MF59;CpG 1826;compound adjuvant;tumor vaccine;MUC1-MBP;dendritic cells
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DOI
PubMed
高影响因子
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
·
2025
·
IF 3.3
Hong-Yu Li,Wei-Lan Zeng,Yi-Wen Ye,Xin Chen,Ming-Ming Zhang,Yi-Si Chen,Cui-Ting Liu,Zhun-Qiang Zhong,Jing Li,Yan Wang
Glia maturation factor-β (Gmfb), an actin filament debrancher, was initially identified in brain and recently linked to liver diseases. To investigate the role of hepatocyte Gmfb (hep-Gmfb) in liver reparative regeneration, hepatocyte-specific gmfb knockout (HepGKO) and overexpression (HepGOE) zebrafish strains were constructed. Both transgenic and wild-type (WT) zebrafish underwent partial hepatectomy (PHX) or were fed high fat, high cholesterol diets to model metabolism-associated steatotic liver disease (MASLD). Under physiological conditions, the HepGKO, HepGOE, and WT fish displayed similar survival, gross appearance, and liver histology. Following PHX, WT liver gmfb levels positively correlated with cell proliferation and proinflammatory cytokine levels. HepGOE showed enhanced regeneration and reduced liver steatosis compared to WT, while HepGKO exhibited opposite effects. In MASLD, WT liver gmfb increased with disease progression. HepGKO experienced worsening liver enlargement, steatosis, ballooning, inflammation, and endoplasmic reticulum stress, while HepGOE showed improvements. HepGOE liver had the highest cell proliferation, but all three groups showed similar levels of cell apoptosis. Moreover, elevated proinflammatory cytokines were observed across MASLD groups, being the highest in HepGKO and lowest in HepGOE. However, stat3 activation was the lowest in HepGKO and highest in HepGOE, while jnk and mapk/erk activation was consistent across the MASLD groups. In il6-treated primary hepatocytes, gmfb abundance influenced stat3 activation, and hep-gmfb abundance significantly affected actin filaments distribution in hepatocytes both in vivo and vitro. Conclusions: Hep-Gmfb boosts regenerative processes by enhancing hepatocyte proliferation, alleviating fatty liver histological abnormalities, and modulating the Il6/Stat3 signaling, potentially through remodeling of actin-filament network within hepatocytes.
研究领域:
分子生物学
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细胞生物学
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肝脏病学
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发育生物学
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遗传学
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信号转导
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病理学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Xia Liu,Nannan Wang,Tingting Cai,Hua Chen,Chunhui Dai,Wanping Zhu
Ethnopharmacological relevance Acute lung injury (ALI), a critical complication of severe pneumonia, lacks targeted therapies. Astilbe chinensis (Maxim.) Franch. & Sav. possesses documented anti-inflammatory and respiratory-protective properties, yet its efficacy against ALI, bioactive constituents, and mechanisms remain unexplored. Aim of the study This study sought to evaluate the therapeutic efficacy and elucidate the mechanisms of action of Astilbe chinensis in the treatment of ALI through the application of network pharmacology and experimental methodologies. Materials and methods UHPLC-MS was used to analyze plasma components absorbed after Astilbe chinensis administration in rats. Inflammation-related targets and pathway enrichment analyses were conducted via network pharmacology technique. Pulmonary function was assessed using forced lung function measurements in a LPS-induced ALI mouse model. ELISA quantified inflammatory mediators, including pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ), chemokines (CCL5, CXCL2), and the anti-inflammatory cytokine IL-10 in mouse lung tissue. Flow cytometry evaluated macrophage polarization, and HE staining examined histopathological changes. qRT-PCR determined the mRNA expression levels of genes like CCR1, IKBKB, CXCL8, STAT3, CXCR4, AKT1, CCL3, CCL5, iNOS, Arg1, YM1 and CCR5, while simple western analysis evaluated the protein expression of t-AKT, p-AKT, t-STAT3, p-STAT3, CCR1 and CCR5 in mouse lung tissues affected by Astilbe chinensis . Results In this study, 20 blood-borne components of Astilbe chinensis were identified, predicted to interact with 369 potential molecular targets, with 331 related to ALI treatment. GO and KEGG pathway analyses showed that 36 targets participate in inflammatory processes, mainly via chemokine signaling pathways. Key targets identified include CCR1, IKBKB, CXCL8, STAT3, CXCR4, AKT1, and CCR5. The principal active constituents of Astilbe chinensis with potential efficacy against ALI were identified as cyclo(phenylalanyl-prolyl), 5-(6-hydroxy-6-methyloctyl)- -2,5-dihydrofuran-2-one, nicotinamide, 3-phenyllactic acid, and phloretin. In vivo studies demonstrated that Astilbe chinensis administration significantly increased M2 macrophage populations in lung tissue while improving forced pulmonary function parameters. Furthermore Astilbe chinensis reduces the levels of inflammatory factors TNF-α, IL-6, IFN-γ, CCL5 (the ligand for CCR5 and CCR1), and the neutrophil chemokine CXCL2 in the lung tissues of ALI mice, while significantly increasing the content of the anti-inflammatory cytokine IL-10. Additionally, Astilbe chinensis significantly downregulated gene expression of chemokine receptors CCR1, CCR5 and their ligands CCL3, CCL5 in ALI mouse lung tissues, while upregulating anti-inflammatory markers Arg1 and Ym1 (M2 macrophage biomarkers). Meanwhile, it exerts a notable inhibitory effect on the protein expression of CCR1, CCR5, p-AKT, and p-STAT3. Conclusion This study demonstrates that Astilbe chinensis significantly improves lung function and pulmonary inflammation in mice with ALI. Component identification combined with network pharmacology analysis reveals that its major anti-inflammatory components are cyclo(phenylalanyl-prolyl), 5-(6-hydroxy-6- -methyloctyl)-2,5-dihydrofuran-2-one, nicotinamide, 3-phenyllactic acid, and phloretin. The anti-inflammatory mechanism may involve inhibiting the gene and protein expression of inflammatory chemokines CCR1 and CCR5, suppressing the activity of the AKT/STAT3 signaling pathway, reducing the expression of inflammatory factors, promoting M2 macrophage polarization, and thereby increasing the release of anti-inflammatory genes and cytokines, ultimately exerting anti-inflammatory effects.
研究领域:
药理学
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民族药理学
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炎症研究
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呼吸系统疾病
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网络生物学
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系统药理学
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免疫学
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DOI
PubMed
高影响因子
CHINESE JOURNAL OF ANALYTICAL CHEMISTRY
·
2025
·
IF 1.3
Jing Gao,Xiaohui Dong,Hang Li,Qing Yang,Wenting Ji,Xianying Lu,Xinyu Chen,Fei Wang,Chaoming Hou
Objective Fujin Shengji (FJSJ) Powder has a positive effect on healing Diabetic Ulcers (DU), but the specific compounds at work have not been identified. Methods Network pharmacology was employed to investigate the primary constituents, potential therapeutic targets, and pharmacological mechanisms of FJSJ Powder treating DU. In vitro experiments were further performed to validate these findings: an LPS-induced RAW264.7 cell model was established to assess the anti-inflammatory effects of FJSJ Powder active constituents treating DU, while a high glucose-induced HUVEC model was cultured to verify the pro angiogenic effect of FJSJ Powder active constituents treating DU. Additionally, the mechanisms by which the optimal active monomers suppress inflammation and enhance angiogenesis in DU were investigated, focusing on the JAK2/STAT3 and PI3K/AKT signaling pathways. Results Network pharmacology identified quercetin (Que), kaempferol (Kae), abietic acid (Aba) and acetyl-11-keto-β-boswellic acid (AKBA) as the primary active constituents of FJSJ Powder treating DU; IL6, TNF, AKT1, and VEGFA were the core targets; and anti-inflammatory effect was mainly enriched in the JAK2/STAT3 signaling pathway, while angiogenesis promotion was mainly enriched in the PI3K/AKT signaling pathway. The vitro experiments have confirmed Que, Kae, Aba, and AKBA could play important roles in anti-inflammatory and angiogenic effects, with AKBA and Aba playing important roles in anti-inflammatory and pro-angiogenic effects, respectively. AKBA can upregulate P-JAK2, P-STAT3, IL-4, and downregulate INOS protein levels to exert anti-inflammatory. Aba can upregulate the P-AKT, P-PI3K, HIF-1α, and VEGFA proteins levels to promote angiogenesis. Conclusion FJSJ Powder promotes DU healing through dual-pathway regulation in anti-inflammatory and pro-angiogenic effects, with AKBA mediating the best anti-inflammatory activity through the JAK2/STAT3 pathway and Aba driving the strongest pro-angiogenic effects via the PI3K/AKT/HIF-1α/VEGFA axis, providing a basis for formula optimization.
研究领域:
药理学
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网络药理学
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中医药
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分子生物学
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创面愈合
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糖尿病并发症
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DOI
高影响因子
Food & Function
·
2023
·
IF 6.1
Jiachen Zhuang,Qianqian Wang,Fei Shen,Jing Wang,Juan Du,Peng Yu,Fengqin Feng,Minjie Zhao
This study investigated the immunomodulatory effects of soft-shelled turtle (Pelodiscus sinensis) peptide (TP) and Chinese pond turtle (Chinemys reevesii) peptide (TMP) on the intestinal mucosal immune system (IMIS). The results demonstrated that TP and TMP improved holistic immunity by restoring the vital immune organ atrophy and proliferation capacity of spleen immune cells. Moreover, TP and TMP significantly increased the serum content of IgA and cytokines that are responsible for immune cell activation and antigen clearance. TP and TMP promoted intestinal B cell activation, class switching recombination, and antibody secreting processes in a T cell-independent manner to increase the SIgA content. Furthermore, TP and TMP enhanced the intestinal barrier by increasing the protein expression of tight junctions (TJs) and adhesion junctions (AJs) and ameliorating the intestinal morphology. Mechanistically, TP and TMP activated the AHR/IL-22/STAT3/IL-6 axis to enhance the IgA response and improve the intestinal barrier, indicating their potential in intestinal health modulation.
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DOI
PubMed
高影响因子
MOLECULAR MEDICINE
·
2025
·Vol. 31
·期 1
·1-17
·
IF 6.4
Liu Jing,Li Wenqi,Jiao Ran,Liu Zhigang,Zhang Tiantian,Chai Dan,Meng Lingxin,Yang Zhongyi,Liu Yuming,Wu Hongliang,Gu Xiaoting,Li Xiaohe,Yang Cheng
Background Cardiac fibrosis is significant global health problem, which is associated with numerous cardiovascular diseases, and ultimately leads to the progression to heart failure. β-adrenergic receptor (β-AR) overactivation play a role in the development of cardiac fibrosis. Miglustat (Mig) has shown anti-fibrosis effects in multiple fibrotic diseases. However, it is unclear whether and how Mig can ameliorate cardiac fibrosis induced by β-AR overactivation. Methods In vivo, mice were injected with isoproterenol (ISO) to induce cardiac fibrosis and treated with Mig. In vitro, primary cardiac fibroblasts were stimulated by ISO and treated with Mig. Levels of cardiac fibrosis, cardiac dysfunction, activation of cardiac fibroblasts were evaluated by real-time polymerase chain reaction, western blots, sirius red staining, immunohistochemistry staining and echocardiography. Through GEO data and knockdown UDP-glucose ceramide glycosyltransferase (UGCG) in primary cardiac fibroblasts, whether Mig alleviates cardiac fibrosis by targeting UGCG was explored. Results The results indicated that Mig alleviated ISO-induced cardiac dysfunction. Consistently, Mig also suppressed ISO-induced cardiac fibrosis. Moreover, Mig attenuated ISO-induced cardiac fibroblasts (CFs) activation. To identify the protective mechanism of Mig on cardiac fibrosis, several classical β-AR downstream signaling pathways, including ERK, STAT3, Akt and GSK3β, were further analyzed. As expected, ISO activated the ERK, STAT3, Akt and GSK3β in both CFs and mouse hearts, but this effect was reversed pretreated with Mig. Besides, Mig ameliorates ISO-induced cardiac fibrosis by targeting UDP-glucose ceramide glycosyltransferase (UGCG) in CFs. Conclusions Mig ameliorates β-AR overactivation-induced cardiac fibrosis by inhibiting ERK, STAT3, Akt and GSK3β signaling and UGCG may be a potential target for the treatment of cardiac fibrosis.
研究领域:
心血管疾病
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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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产品关联
DOI
PubMed
高影响因子
Science Signaling
·
2020
·Vol. 13
·期 646
·
IF 6.467
Xiao-Wei Gu,Zi-Cong Chen,Zhen-Shan Yang,Yan Yang,Ya-Ping Yan,Yue-Fang Liu,Ji-Min Pan,Ren-Wei Su,Zeng-Ming Yang
Embryo implantation involves a sterile inflammatory reaction that is required for the invasion of the blastocyst into the decidua. Adenosine triphosphate (ATP) released from stressed or injured cells acts as an important signaling molecule to regulate many key physiological events, including sterile inflammation. We found that the amount of ATP in the uterine luminal fluid of mice increased during the peri-implantation period, and this depended on the presence of an embryo. We further showed that the release of ATP from receptive epithelial cells was likely stimulated by lactate released from the blastocyst through connexin hemichannels. The ATP receptor P2y2 was present on uterine epithelial cells during the preimplantation period and increased in the stromal cells during the time at which decidualization began. Pharmacological inhibition of P2y2 compromised decidualization and implantation. ATP-P2y2 signaling stimulated the phosphorylation of Stat3 in uterine luminal epithelial cells and the expression of early growth response 1 ( Egr1 ) and prostaglandin-endoperoxide synthase 2 ( Ptgs2, also known as Cox-2 ), all of which are required for decidualization and/or implantation, in stromal cells. Short exposure to high concentrations of ATP promoted decidualization of primary stromal cells, but longer exposures or lower ATP concentrations did not. The expression of genes encoding ATP-degrading ectonucleotidases increased in the decidua during the peri-implantation period, suggesting that they may limit the duration of the ATP signal. Together, our results indicate that the blastocyst-induced release of ATP from uterine epithelial cells during the peri-implantation period may be important for the initiation of stromal cell decidualization.
研究领域:
生殖生物学
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发育生物学
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细胞信号转导
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分子胚胎学
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免疫学（无菌性炎症）
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DOI
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2024
·Vol. 22
·期 1
·1-21
·
IF 10.6
Chen Shang,He Yan,Huang Xin,Shen Yao,Zou Qingshuang,Yang Gun,Fu Li,Liu Quan,Luo Dixian
Tumor-associated macrophages (TAMs) are a promising target for cancer immunotherapy, but delivering therapeutic agents to TAMs within the tumor microenvironment (TME) is challenging. In this study, a photosensitive, dual-targeting nanoparticle system (M.RGD@Cr-CTS-siYTHDF1 NPs) was developed. The structure includes a shell of DSPE-modified RGD peptides targeting integrin receptors on tumor cells and carboxymethyl mannose targeting CD206 receptors on macrophages, with a core of chitosan adsorbing m6A reading protein YTHDF1 siRNA and chromium nanoparticles (Cr NPs). The approach is specifically designed to target TAM and cancer cells, utilizing the photothermal effect of Cr NPs to disrupt the TME and deliver siYTHDF1 to TAM. In experiments with tumor-bearing mice, M.RGD@Cr-CTS-siYTHDF1 NPs, when exposed to laser irradiation, effectively killed tumor cells, disrupted the TME, delivered siYTHDF1 to TAMs, silenced the YTHDF1 gene, and shifted the STAT3-STAT1 equilibrium by reducing STAT3 and enhancing STAT1 expression. This reprogramming of TAMs towards an anti-tumor phenotype led to a pro-immunogenic TME state. The strategy also suppressed immunosuppressive IL-10 production, increased expression of immunostimulatory factors (IL-12 and IFN-γ), boosted CD8 + T cell infiltration and M1-type TAMs, and reduced Tregs and M2-type TAMs within the TME. In conclusion, the dual-targeting M.RGD@Cr-CTS-siYTHDF1 NPs, integrating dual-targeting capabilities with photothermal therapy (PTT) and RNA interference, offer a promising approach for molecular targeted cancer immunotherapy with potential for clinical application. Graphical Abstract
研究领域:
癌症生物学
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纳米技术
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免疫疗法
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分子生物学
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药理学
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DOI
PubMed
高影响因子
ACS Nano
·
2024
·
IF 15.8
Hao Wu,Changcheng Chen,Jiangfeng Li,Dongmei Yu,Xun Wu,Hai Huang,Zhen Tang,Qi Wu,Shichao Yan,Ning Wang,Mo Wang,Feilong Wei,Yunlong Yu,Duan Wang,Mengting Shi,Xusong Yue,Pengfei Cao,Zenghui Zheng,Xiaokang Li,Baolin Guo,Lei Shi,Zheng Guo
Infectious bone defects pose significant clinical challenges due to persistent infection and impaired bone healing. Icam1+ macrophages were identified as crucial and previously unrecognized regulators in the repair of bone defects, where impaired oxidative phosphorylation within this macrophage subset represents a significant barrier to effective bone regeneration. To address this challenge, dual-responsive iron-doped barium titanate (BFTO) nanoparticles were synthesized with magnetic and ultrasonic properties. These nanoparticles were further loaded with the anti-inflammatory agent curcumin and coated with engineered mesenchymal stem cell membranes (EMM) modified with γ3 peptide, creating BFTO-Cur@EMM nanoparticles specifically designed to target Icam1+ macrophages. These nanoparticles were shown to disrupt bacterial biofilms under alternating magnetic fields (AMF) and to activate oxidative phosphorylation and osteogenic immune responses in Icam1+ macrophages via low-intensity pulsed ultrasound (LIPUS). Transcriptomic sequencing and validation experiments demonstrated that this approach activates oxidative phosphorylation (OXPHOS) by stimulating the JAK2-STAT3 pathway and inhibiting the MAPK-JNK pathway, thereby promoting the polarization of Icam1+ macrophages toward a pro-reparative phenotype and enhancing the secretion of pro-angiogenic and osteogenic cytokines. These nanoparticles were subsequently integrated into quaternized chitosan (QCS) and tricalcium phosphate (TCP) to create a bioink for three-dimensional (3D) printing anti-infection QT/BFTO-Cur@EMM bone repair scaffolds. In vivo studies indicated that these scaffolds significantly improved the healing of infectious bone defects without causing thermal damage to surrounding tissues. This work highlights the potential of this material and the targeting of Icam1+ macrophages as an effective strategy for simultaneously controlling infection and promoting bone regeneration.
研究领域:
生物材料
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纳米技术
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骨科
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免疫学
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再生医学
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DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2024
·
IF 10.5
Jun Zhang,Lei Su,Zhinan Liu,Jincheng Tang,Lichen Zhang,Ziang Li,Dong Zhou,Zhuo Sun,Kun Xi,Peirong Lu,Guohua Deng
Following an ocular chemical injury, the release of neutrophil extracellular traps (NETs) triggers an innate immune cascade fibrotic effect involving macrophages (Mø), which limits corneal repair. However, the interplay and mechanisms between NETs and macrophages, as well as the coordination between the innate immunity and corneal repair, remain challenging issues. Using a co-culture system, we report that chemical stimulation exacerbates the accumulation of reactive oxygen species (ROS) within the polymorphonuclear neutrophils, leading to NET formation and the activation of M2 macrophages, ultimately inducing pathological fibrosis of the ocular surface through the IL-10/STAT3/TGF-β1/Smad2 axis. Inspired by the locally formed acidic microenvironment mediated by innate acute inflammatory stimulation, we further integrate sericin with oxidized chitosan nanoparticles loaded with black phosphorus quantum dots (BPQDs) using Schiff base chemistry to construct a functional pH-responsive hydrogel. Following corneal injury , the hydrogel selectively releases BPQDs in response to the acidic environment, inhibiting the innate immune cascade fibrosis triggered by the PMN-ROS-NETs. Thus, corneal pathological fibrosis is alleviated and reshaping of the ocular surface takes place. These results represent a refinement of the mechanism of inherent immune effector cell interactions, and provide new research ideas for the construction of nano biomaterials that regulate pathological fibrosis.
研究领域:
生物材料
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免疫学
·
眼科
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组织工程
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纳米技术
✓ 已验证
DOI
PubMed
高影响因子
Heliyon
·
2023
·
IF 4
Lingling Song,Jian Xu,Yanqiong Shi,Hemiao Zhao,Min Zhang,Yuefei Wang,Ying Cui,Xin Chai
Febrile seizures (FS) are the most common type of seizures for children. As a commonly used representative cold formula for resuscitation, Zixue Powder (ZP) has shown great efficacy for the treatment of FS in clinic, while its active ingredients and underlying mechanism remain largely unclear. This study aimed to preliminarily elucidate the material basis of ZP and the potential mechanism for the treatment of FS through ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS), network pharmacology, and molecular docking. UPLC-Q-TOF-MS was firstly applied to characterize the ingredients in ZP, followed by network pharmacology to explore the potential bioactive ingredients and pathways of ZP against FS. Furthermore, molecular docking technique was employed to verify the binding affinity between the screened active ingredients and targets. As a result, 75 ingredients were identified, containing flavonoids, chromogenic ketones, triterpenes and their saponins, organic acids, etc. Through the current study, we focused on 13 potential active ingredients and 14 key potential anti-FS targets of ZP, such as IL6, STAT3, TNF, and MMP9. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that inflammatory response, EGFR tyrosine kinase inhibitor resistance, AGE-RAGE signaling pathway in diabetic complications, and neuroactive ligand-receptor interaction were the main anti-FS signaling pathways. Licochalcones A and B, 26-deoxycimicifugoside, and hederagenin were screened as the main potential active ingredients by molecular docking. In conclusion, this study provides an effective in-depth investigation of the chemical composition, potential bioactive components, and possible anti-FS mechanism of ZP, which lays the foundation for pharmacodynamic studies and clinical applications of ZP.
研究领域:
药理学
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分析化学
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神经科学
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中医中药
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DOI
高影响因子
危险品化学品经营许可证（带存储）