JOURNAL OF ETHNOPHARMACOLOGY
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2024
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IF 4.8
Zhangjie Wu,Ying Yin,Ruiyi Liu,Xianhui Li,Yan Sun,Suk-yu Yau,Lei Wu,Yan Liu,Miroslav Adzic,Hailou Zhang,Gang Chen
Ethnopharmacological relevance Jiawei-Xiaoyao Pill (JWX), a classic formula in traditional Chinese medicine, is derived from Xiaoyao Pill by adding significant amounts of Gardeniae Fructus (GF) and Moutan Cortex (MC). It is frequently used for the treatment of depression. JWX has been demonstrated to uniquely elicit rapid antidepressant-like effects within the prescribed dosage range. To date, GF has been shown to have rapid antidepressant-like effects, but a much higher dose is required than its proportion in JWX. It is assumed that the synergism of GF with a minimum number of other herbs in JWX serves as a refined formula that exerts these rapid antidepressant-like effects. Identification of a refined formula is important for prioritizing the herbs and ingredients to optimize the quality control of JWX. However, such a refined formula for JWX has not been identified yet Aim of the study Here we aimed to identify a refined formula derived from JWX for optimized rapid antidepressant-like effects. Since the neuroinflammation mechanism involving in depression treatment has not been previously investigated for JWX, we tested the mechanism for both JWX and the refined formula Materials and methods Individual herbs (MC ; ASR, Angelica Sinensis Radix; Bupleuri Radix; Paeonia Radix Alba ) that show antidepressant-like responses were mixed with GF at the proportional dosage in JWX to identify the refined formula. Rapid antidepressant-like effects were assessed by using NSF (Novelty Suppressed Feeding Test) and other behavioral tests following a single administration. The identified formula was further tested using a lipopolysaccharide (LPS)-induced depressive model, and the molecular signaling mechanisms were investigated using western blot analysis, immunofluorescence, and pharmacological inhibition of mTOR signaling. Scopolamine (Scop) is used as a positive control for induction of rapid antidepressant effects Results A combination of GF, MC and ASR (GMA) at their dosages proportional to JWX induced behavioral signs of rapid antidepressant-like responses in both normal and LPS-treated mice, with the antidepressant-like effects sustained for 5 d. Similar to JWX or Scop, GMA rapidly reduced the neuroinflammation signaling of Iba-1-NF-кB, enhanced neuroplasticity signaling of CaMKII-mTOR-BDNF, and attenuated the upregulated expressions of the NMDAR sub-units GluN1 and GluN2B in the hippocampus of LPS-treated mice. GMA, JWX and Scop rapidly restored the number of BDNF-positive cells reduced by LPS treatment, in the CA3 region of the hippocampus. Furthermore, rapamycin, a selective inhibitor of mTOR, blunted the rapid antidepressant-like effects and hippocampal BDNF signaling upregulation by GMA Conclusion GMA may serve as a refined formula from JWX, capable of inducing rapid antidepressant-like effects. In LPS-induced depression model, the effects of GMA were mediated via rapidly alleviating neuroinflammation and enhancing neuroplasticity
研究领域:
药理学
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神经科学
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中医
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行为科学
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DOI
PubMed
高影响因子
MICROBIAL PATHOGENESIS
·
2024
·
IF 3.3
Xiaoye Cheng,Yijin Jiang,Xu Zhao,Nana Ma,Xiangzhen Shen
Lactate has been increasingly recognized for its role in diseases progression, necessitating a deeper understanding of its metabolic processes and regulatory mechanisms. This study aimed to evaluate the impact of lipopolysaccharide (LPS) on lactate accumulation in bovine mammary epithelial cells (BMECs) and to elucidate the underlying regulatory mechanisms. Further optimization of LPS treatment points was achieved by assessing the content of key glycolytic enzymes-hexokinases (HK), pyruvate kinase (PK) and pyruvate dehydrogenase (PDH)-as well as the expression levels of HK2, pyruvate dehydrogenase kinase4 (PDK4) and lactate dehydrogenase (LDHA). Our results indicate that LPS can promote intracellular glycolysis and inhibits pyruvate synthesis, thereby increasing lactate content. BMECs were cultured and divided into a control group (CON) and an LPS-stimulated group (10 μg/mL for 6 h, LPS group). LPS was found to upregulate expression levels of HIF-1α and MCT1, suggesting a role for HIF-1α and MCT1 in cellular glucose metabolism. To explore the effect of HIF-1α on lactate accumulation, BMECs were stimulated with a HIF-1α inducer (COCL 2 ) and HIF-1α inhibitor (DMBPA). COCL 2 was observed to promote lactate accumulation, while DMBPA inhibited it. Additionally, modulation of HIF-1α expression influenced the expression of MCT1, which is a crucial transporter for extracellular lactate influx. To investigate the specific impact of MCT1 on intracellular lactate, we utilized overexpression plasmids and small interfering RNA to modulate MCT1 expression. The findings indicate that while MCT1 expression alone does not affect intracellular lactate levels, it does modulate the changes induced by LPS. In conclusion, our study suggests that LPS regulates lactate accumulation in BMECs through the HIF-1α/MCT1 pathway, providing insights into the metabolic dysregulation associated with LPS-induced stress in dairy cattle.
研究领域:
动物科学
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细胞生物学
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代谢学
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乳品科学
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DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2022
·
IF 6.656
Zhenhao Li,Haitao Pan,Jihong Yang,Dongjie Chen,Yu Wang,Han Zhang,Yiyu Cheng
Background Xuanfei Baidu Formula (XBF) is an effective traditional Chinese medicine (TCM) remedy for treating coronavirus disease 2019 (COVID-19) in China. This herbal medicine has shown effects in reducing clinical symptoms and shortening the average length of hospital stay for COVID-19 patients. Previous studies have demonstrated that XBF alleviates acute lung injury (ALI) by regulating macrophage-mediated immune inflammation, but the mechanisms of action remain elusive. Purpose This study aimed to evaluate the lung-protective and anti-inflammatory effects of XBF and its underlying mechanisms. Methods Here, XBF's effects were investigated in an ALI mouse model induced by inhalation of atomized lipopolysaccharide (LPS). Besides, the LPS-induced inflammation model in RAW264.7 cells was used to clarify the underlying mechanisms of XBF against ALI. Results Our results showed that XBF treatment alleviated LPS-induced lung injury, as evidenced by reduced histopathological changes, pulmonary alveoli permeability, fibrosis, and apoptosis in the lung tissues. In addition, inflammation was alleviated as shown by decreased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β in serum and bronchoalveolar lavage fluid (BALF), and reduced white blood cell (WBC) count in BALF. Furthermore, consistent with the in vivo assay, XBF inhibited LPS-induced inflammatory cytokines release and pro-inflammatory polarization in RAW264.7 cells. Mechanistically, XBF increased mitochondrial fusion by upregulating Mfn1 and attenuated NLRP3 inflammasome activation by repressing Casp11, respectively, to inhibit NF-κB and MAPK pathways, thus repressing pro-inflammatory macrophage polarization. Conclusion In this study, we demonstrate that XBF exerts anti-ALI and -inflammatory effects by recovering mitochondrial dynamics and reducing inflammasome activation, providing a biological illustration of the clinical efficacy of XBF in treating COVID-19 patients.
研究领域:
药理学
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免疫学
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细胞生物学
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中医
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DOI
PubMed
高影响因子
CHEMISTRY & BIODIVERSITY
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2025
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IF 2.5
Zebin Huang,Wanying Zhang,Qi Shu,Xiao-Chun Guo,Xi Zheng,YuJing Lu
Inflammation is an important predisposing factor for many chronic diseases. The dietary flavonoid silibinin has excellent anti-inflammatory properties in cells, but its low bioavailability in the blood compromises its therapeutic potential. This study aims to investigate the potential of dibenzoylmethane (DBM) to synergistically enhance the anti-inflammatory benefits of silibinin (SB). The synergistic effects of DBM and SB in combination were evaluated in LPS-induced RAW264.7 cells and TPA-induced mice. In addition, a network pharmacology approach and molecular docking were used to explore the key targets and signaling pathways of DBM and SB in combination. The results showed that DBM and SB synergistically inhibited the production of NO, ROS, IL-1β, and TNF-α in a 1:1 concentration ratio. These two compounds may exert their synergistic effects by modulating the NF-κB and HIF-1 signaling pathways, among others. Molecular docking revealed that both compounds exhibited high binding affinities to iNOS and COX-2. Compared with single compound use, the two compounds in combination significantly reduced ear edema and inflammatory cell infiltration, and inhibited the protein expression of iNOS and COX-2 in TPA-induced mice. This research provides a rationale for the combination of DBM and SB as an effective anti-inflammatory agent.
研究领域:
药理学
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免疫学
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分子生物学
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炎症研究
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产品关联
DOI
PubMed
高影响因子
Journal of Hard Tissue Biology
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2022
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IF 0.593
Jie Zhang,Yongli Wang,Jianzhong Zhang,Shaoyan Huang
We investigated the anti-inflammatory effect of hydroxyethyl starch (HES) 6% 200/0.5 on lipopolysaccharide (LPS)-induced RAW264.7 cells based on the high mobility group protein B1/nuclear transcription factor-κB (HMGB1/NF-κB) signaling pathway. The mouse monocyte macrophage RAW264.7 cells were divided into control group (no additional treatment), LPS group (0.2 pg/ml LPS), LPS+HES group (0.2 pg/ml LPS+6% HES) and LPS+TAK-242 (HMGB1/NF-κB signal pathway blocker) group (0.2 pg/ml LPS The LPS+HES+TAK-242 group (0.2 pg/ml LPS+6% HES+1 μ mol/l TAK-242) was cultured for 48 hours. Griess method and ELISA were used to detect the levels of nitric oxide (NO), tumor necrosis factor α (TNF-α), interleukin (IL)-6 and IL-1β in cell supernatant. The level of intracellular reactive oxygen species (ROS) was detected by flow cytometry. The mitochondrial membrane potential was detected by immunofluorescence. The mRNA expressions of inducible nitric oxide synthase (iNOS), HMGB1, Toll-like receptor 4 (TLR4), nuclear factor-κ b inhibitory protein α (IκBα) and NF-κB were detected by qRT-PCR. The expressions of HMGB1, TLR4, IκBα, phosphorylated IκBα (p-IκBα), NF-κB and phosphorylated NF-κB (p-NF-κB) were detected by western blotting. Compared with the control group, the expression levels of NO, TNF-α, IL-6, IL-1β, ROS, iNOS, HMGB1, TLR4, NF-κB mRNA, HMGB1, TLR4 and p-NF-κB proteins in the LPS group, LPS+HES group, LPS+TAK-242 group and LPS+HES+TAK-242 group increased (P<0.05), the expression levels of mitochondrial membrane potential, IκBα mRNA and p-IκBα protein decreased (P<0.05). Compared with LPS group, the expression levels of NO, TNF-α, IL-6, IL-1β, ROS, iNOS, HMGB1, TLR4, NF-κB mRNA, HMGB1, TLR4 and p-NF-κB proteins in the LPS+HES group, LPS+TAK-242 group and LPS+HES+TAK-242 group increased (P<0.05), the expression levels of mitochondrial membrane potential, IκBα mRNA and p-IκBα protein decreased (P<0.05). The expression levels of mitochondrial membrane potential, IκBα mRNA and p-IκBα protein increased (P<0.05). Six % HES 200/0.5 could down-regulate the expression of molecules related to HMGB1/NF-кB signaling pathway, and reduce the inflammatory response of RAW264.7 cells induced by LPS.
研究领域:
药理学
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免疫学
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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
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2017
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IF 2.956
Xiaobao Gong,You Yang,Ligua Huang,Qingyan Zhang,Rong-Zhen Wan,Peng Zhang,Baoshun Zhang
To evaluate the hepatoprotective effects and potential mechanisms of paeonol (Pae) against acute liver failure (ALF) induced by lipopolysaccharide (LPS)/ d -galactosamine ( d -GalN) in mice, we examined anti-oxidative, anti-inflammatory and anti-apoptotic activities of Pae. We found that Pae pretreatment markedly reduced the activities of alanine transaminase and aspartate transaminase as well as the histopathological changes induced by LPS/ d -GalN. Catalase , glutathione and superoxide dismutase activities increased and reactive oxygen species activity decreased after Pae treatment compared with LPS/ d -GalN treatment. Pretreatment with Pae also significantly inhibited the expression levels of iNOS, nitric oxide (NO), COX-2 and prostaglandin E 2 (PGE 2 ). In addition, Pae administration prevented the phosphorylated expression of IκB kinase, inhibitor kappa B in the nuclear factor-kappa B (NF-κB) signaling pathway , and suppressed the phosphorylated expression of extracellular signal-regulated kinase (ERK), c-jun-N-terminal kinase and p38 in the MAPK signaling pathway. Pretreatment with Pae also inhibited hepatocyte apoptosis by reducing the expression of caspases 3, 8, 9, and Bax, and increasing Bcl-2. In total, protective effects of Pae against LPS/ d -GalN-induced ALF in mice are attributed to its antioxidative effect, inflammatory suppression in NF-κB and MARK signaling pathways, and inhibition of hepatocyte apoptosis inhibition. Therefore, Pae can be a potential therapeutic agent in attenuating LPS/ d -GalN-induced ALF in the future.
研究领域:
药理学
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肝病学
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免疫学
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分子生物学
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DOI
PubMed
高影响因子
NEUROCHEMICAL RESEARCH
·
2026
·Vol. 51
·期 4
·232
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IF 4.5
Zhang Xinfeng,Lian Zhuo,Lei Sijie,Yi Tanhui,Zhao Shuyin,Liu Mingxiang,Gui Yiling,Zhu Chengyi,Xie Qian,Ma Rong
The selection of appropriate in vitro inflammatory models is critical for mechanistic studies of neuroinflammation and the screening of anti-inflammatory therapeutics. Lipopolysaccharide (LPS) combined with interferon-γ (IFN-γ) and LPS combined with adenosine triphosphate (ATP) are widely used to induce microglial inflammation; however, their distinct phenotypic characteristics and optimal applications have not been systematically compared. In this study, we combined transcriptomic profiling with functional assays to compare these two inflammatory paradigms in BV2 microglia. Our results showed that both models activated the chemokine–cytokine inflammatory network and induced the production of inflammatory mediators and chemokines, but exhibited distinct molecular and functional biases. LPS/IFN-γ stimulation preferentially upregulated genes such as Lcn2 , Ccl2 , Upp1 , and Pim2 , which are associated with innate immune activation, chemokine-mediated inflammatory responses, and cell survival signaling, and was accompanied by marked increases in NO and TNF-α production. In contrast, the LPS/ATP model preferentially upregulated genes associated with ECM/cell adhesion, inflammatory and cellular homeostatic regulation, oxidative stress, and calcium-dependent secretion, including Thbs1 , Thbd , Srxn1 , Syt7 , and Procr . Functionally, this model exhibited more pronounced IL-1β maturation and release, relatively lower NO production, and greater mitochondrial dysfunction and cell injury. Pharmacological inhibition of NLRP3 with MCC950 significantly attenuated ATP-induced IL-1β maturation, supporting the involvement of the NLRP3 inflammasome in the LPS/ATP model. Overall, the LPS/IFN-γ model is more suitable for investigating the NO/iNOS–TNF-α axis, IFN-γ-mediated synergistic pro-inflammatory responses, and classical pro-inflammatory activation, as well as for screening anti-inflammatory agents. In contrast, the LPS/ATP model is more appropriate for studying IL-1β maturation and release, NLRP3 inflammasome activation, mitochondrial damage, and inflammation-related cell death, as well as for screening inflammasome inhibitors. Our findings provide an empirical framework for rational model selection in microglial inflammation research.
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高影响因子
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
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2022
·Vol. 395
·期 10
·1283-1295
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IF 3.195
Xiong Ziwei,Cui Yushun,Wu Jiahui,Shi Lingyu,Quan Wen,Yang Shilin,Feng Yulin
Pteris cretica L. var. nervosa is one of the most well-known Chinese medicines. Although it is widely used to treat jaundice hepatitis, the main ingredient for its treatment was not thoroughly explored until recently. Essentially, the purpose of this study is to find the monomer compound in Pteris cretica L. var. nervosa , which is most likely to be effective in treating liver injury. Through the model of LPS/D-gal-induced liver injury in mice, the best therapeutic site of the total extract was explored, the chemical components of the parts with the best therapeutic effect were separated, a total of 10 flavonoids were isolated, and the RAW264.7 cells induced by LPS were used as the experimental model to explore the preliminary anti-inflammatory activity of NO production in vitro. Finally, the anti-inflammatory activity and the highest content in this plant Luteolin-7-O-rutinoside (LUT) were selected, as the object of study in vivo. It was found that LUT could not only reduce alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, but also significantly reduce the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), and inhibit PI3K/AKT/AMPK/NF-κB pathway. In addition, LUT can increase levels of SOD and GSH to reduce oxidative stress. It has an obvious therapeutic effect on acute liver injury induced by LPS/D-gal in mice. Therefore, infer LUT is a functional substance in Pteris cretica L. var. nervosa. Graphical abstract
研究领域:
药理学
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免疫学
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肝脏病学
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分子生物学
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DOI
PubMed
高影响因子
Oncology Letters
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2022
·Vol. 23
·期 6
·1-11
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IF 3.111
Chi-Ming Liu,Lijie An,Zhengping Wu,Ai-Jun Ouyang,Mengqiao Su,Zichen Shao,Yi Lin,Xiaoyu Liu,Yinjie Jiang
6‑Gingerol is a bioactive compound isolated from Zingiber officinale. 6‑Gingerol has been shown to have anticancer effects in numerous types of cancer cell. The mechanisms underlying the anticancer effect of 6‑Gingerol in prostate cancer requires investigation. In the present study, the effect on cell viability of 6‑Gingerol on LNCaP, PC3 and DU145 prostate cancer cells were determined using the MTT and colony formation assays. 6‑Gingerol significantly inhibited cell migration, adhesion and invasion in LPS‑stimulated and LPS‑unstimulated prostate cancer cells. Furthermore, these changes were accompanied by alterations in the protein expression levels of epithelial‑mesenchymal transition biomarkers, including E‑cadherin, N‑cadherin, Vimentin and zonula occludens‑1. 6‑Gingerol also induced autophagy by significantly increasing LC3B‑Ⅱ and Beclin‑1 protein expression levels in prostate cancer cells. Combining 6‑Gingerol with LY294002, an autophagy inhibitor, significantly increased cell survival in DU145 cells. Furthermore, 6‑Gingerol significantly decreased the protein expression levels of glutathione (GSH) peroxidase 4 and nuclear factor erythroid 2‑related factor 2 in prostate cancer cells. Reactive oxygen species (ROS) levels were significantly increased but GSH levels were decreased following 6‑Gingerol treatment in prostate cancer cells. Co‑treatment with the ferroptosis inhibitor, ferrostatin‑1, significantly increased cell viability and significantly decreased ROS levels in 6‑Gingerol‑treated cells. These results suggested that 6‑Gingerol may have inhibited prostate cell cancer viability via the regulation of autophagy and ferroptosis. In addition, 6‑Gingerol inhibited cell migration, adhesion and invasion via the regulation of EMT‑related protein expression levels in LPS‑stimulated and LPS-unstimulated prostate cancer cells. In conclusion, 6‑Gingerol may induce protective autophagy, autophagic cell death and ferroptosis‑mediated cell death in prostate cancer cells. These findings may provide a strategy for the treatment and prevention of prostate cancer.
研究领域:
肿瘤学
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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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DOI
PubMed
高影响因子
NEW JOURNAL OF CHEMISTRY
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2025
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IF 2.5
Shipeng Jiang,Siyu Han,Xinyi Wang,Yueran Ma,Yue Chen,Mingyang Sun,Peiran Meng,Shaokai Du,Yue Sun
Rapid and portable lipopolysaccharide (LPS) detection is of great clinical significance. In this study, a paper-based (PB) sensor for rapid LPS detection was developed based on a smartphone and ultrafast atom transfer radical polymerization (UATRP). First, the filter paper (FB) was modified with chitosan (CS) and glutaraldehyde (GA). LPS was modified onto FB using an amino aptamer (Apt), and this cis-diol site from LPS was selectively cross-linked with the boronic acid group of the initiator 4-(bromomethyl) phenylboronic acid (BPA). Then, UATRP was performed using carbon quantum dots (CQDs) as the catalyst and methacrolein (MLA) as the functional monomer, to generate aldehyde-rich polymer brushes on filter paper. After the efficient covalent conjugation of abundant aldehyde groups with chlorinated Nile blue (CNB), the paper-based sensor was successfully prepared. RGB values were obtained by a smartphone application (App) for analysis. Under the optimized experimental conditions, the developed sensor demonstrated good performance compared to other PB-based sensors. It achieved a lower detection limit (LOD) of 22.86 pg mL−1 (S/N = 3) and exhibited a wider linear detection range (1.0 × 102 to 1.0 × 108 pg mL−1). Importantly, the sensor exhibited both high selectivity and remarkable operational stability during LPS detection. These results not only validate the sensor's analytical reliability but also provide a strong foundation for clinical applications and broader biomedical uses.
研究领域:
生物医学工程
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分析化学
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临床诊断学
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纳米生物技术
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转化医学
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产品关联
DOI
高影响因子
Advanced Healthcare Materials
·
2021
·Vol. 11
·期 8
·2102271
·
IF 9.933
Yu-Wei Zhou,Yu Wu
Macrophages settle in heterogeneous microenvironments rendered by other cells and extracellular matrices. It is well known that chemical stimuli direct macrophage behavior; however, the contributions of viscosity, which increases in inflammatory tissues but not in tumors, are ignored in immune responses including effective activation and timely attenuation. This paper demonstrates that transient lipopolysaccharide (LPS)-treated macrophages benefit from elastic substrates, whereas viscoelastic substrates with similar storage moduli support the inflammatory responses of macrophages under persistent stimulations and consequently amplify the distinctions between the transient and persistent LPS-induced transcriptional programs. Actin filaments (F-actin) fluctuate in line with transcriptional profiles and can be mathematically predicted by a clutch-like model. Moreover, viscosity modifies immune responses through transcription factors NF- κ B and C/EBP δ , which act as switches discriminating transient and persistent infections. Interestingly, enhanced immune responses, consistent with the lower activated states, are attenuated promptly by the actin nucleation-related translocation of ATF3 to nuclei. These findings suggest that the substrate viscoelasticity induces more intense inflammation only in the case of persistent infection and promotes more sensitively perceiving the duration of infection through the F-actin correlated transcription factors. In addition, it may facilitate the cognition of immune response in inflammatory and cancerous microenvironments and have a wide range of applications in inflammatory regulations.
研究领域:
免疫学
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细胞生物学
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生物物理学
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炎症
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组织工程
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DOI
PubMed
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
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2025
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IF 3.6
Li ChenQi,Miao Gen,Shi Wenjing,Gu Yangjuan,Li Weiwei,Cai Mengyu,Qu Yicui,Tang Yuxiao,Lu Hongtao,Li Hongxia,Shen Hui
The neuroinflammation plays a crucial role in the pathogenesis and progression of depression. Microglia serve as the principal source of neuroinflammatory factors and regulate neuroinflammation via M1 and M2 polarization phenotypes. Moreover, NOD like receptor protein 3 (NLRP3) inflammasome pathway is considered to be important in regulating pro-inflammatory cytokine release in the hippocampus. Zinc supplementation has been shown to effectively alleviate depressive symptoms in patients. In this study, we utilized a lipopolysaccharide (LPS)-induced mouse model of depression and LPS-activated BV-2 cells to examine the impact of zinc supplementation. The findings indicated that zinc supplementation could: (1) ameliorate the depressive-like behaviors of the mouse model with inhibition of inflammatory cytokines and zinc homeostasis recovery. (2) induce the polarization of microglia towards the M2 phenotype in vivo and in vitro. (3) suppress the activation of the NLRP3 inflammasome pathway by impeding the expression of P2X purinergic receptor 7 (P2 × 7) induced by LPS, thereby regulating microglial polarization. This may represent a crucial pathway via which zinc inhibits the M1 polarization of microglia, promotes polarization towards the M2 phenotype, thus improving neuroinflammation and exerting an antidepressant effect.
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PubMed
高影响因子
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