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Looking for the health topic Inflammation? View in Explore →

Found 18 results for "Inflammation"

Articles (6)

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Abstracts (6)

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Paeoniflorin alleviates anxiety-like behaviors in sleep-deprived male mice by suppressing inflammation of the paraventricular nucleus of the hypothalamus.

<p>BACKGROUND: Insomnia represents a major global health challenge, with profound detrimental effects on physical and mental well-being. Paeoniflorin (PF), a bioactive component derived from Paeonia lactiflora Pall. (known as "Shao Yao" in traditional Chinese medicine, TCM), has garnered growing interest for its potential in the management of mental disorders. PURPOSE: The present study was designed to: 1) evaluate the effects of PF on anxiety-like behaviors, body weight changes, and the levels of inflammatory factors in sleep-deprived (SD) mice; 2) determine its optimal therapeutic dose; and 3) explore the underlying mechanisms of action. METHODS: Male C57BL/6 mice (n=8 per group) were randomly divided into six experimental groups: Control, SD + Saline, SD + 15 mg/kg PF, SD + 30 mg/kg PF, SD + 60 mg/kg PF, and SD + 0.5 mg/kg Diazepam (DZP). Mice in the PF-treated groups received daily intraperitoneal injections of PF for the entire duration of the SD protocol. To identify the brain regions targeted by PF, c-Fos immunofluorescence staining and chemogenetic approaches were employed. Additionally, network pharmacology, molecular docking, and molecular dynamics simulations were utilized to predict and validate the potential molecular targets of PF. Finally, the western blot experiment was used for verification. RESULTS: This study demonstrated that PF effectively attenuated anxiety-like behaviors in SD mice. Mechanistically, this beneficial effect was associated with the inhibition of three key pathological processes in SD mice: excessive activation of the paraventricular nucleus of the hypothalamus (PVN), aberrant phosphorylation of the epidermal growth factor receptor/phosphatidylinositol 3-kinase/protein kinase B (EGFR/PI3K/AKT) signaling pathway, and abnormally elevated inflammatory responses. CONCLUSION: PF alleviates SD-induced anxiety by curbing PVN hyperactivity, EGFR/PI3K/AKT hyper-phosphorylation and neuroinflammation, offering a multi-target therapeutic strategy for SD-related disorders.</p>

Gong H, Wu Z, Liu R, Zhang Y, Song D, Wang M, Li X, Wu Y, Zhao M, Feng B, Zhao Z, Zhang K, Phytomedicine : international journal of phytotherapy and phytopharmacology
Animal Study

Asiaticoside Alleviates Alzheimer's Disease by Regulating PPP1CC Expression to Suppress Inflammation and Mitochondrial Dysfunction.

<p>OBJECTIVE: Alzheimer's disease (AD) is a neurodegenerative disorder. Asiaticoside (AS), one of the main active components of Centella asiatica, shows therapeutic potential in various diseases, including AD. However, the specific molecular mechanisms by which AS treats AD remain unclear. METHODS: Cell counting kit-8 (CCK-8) and flow cytometry were used to assess cell viability, apoptosis, and changes in JC-1 mitochondrial membrane potential. Western blot (WB) was used to detect protein expression. The ferrous ion fluorescence assay kit was used to measure Fe2+ levels. Enzyme-linked immunosorbent assay (ELISA) kits were used to detect interleukin-1β (IL-1β) and IL-6 levels. GeneCards, comparative toxicogenomics database (CTD), and swisstargetprediction databases were used to obtain AD and AS targets. Enrichment analysis and plotting were performed using the clusterProfiler package in R. The simplified molecular input line entry system (SMILES) website was used to obtain the 3D structure of AS. The universal protein resource (UniProt) website was used to obtain the protein structure of protein phosphatase 1 catalytic subunit gamma (PPP1CC). Autodock v4.2.6 was used for molecular docking. RESULTS: AS improved cell viability in amyloid β1-42 (Aβ1-42)-induced human brain microvascular endothelial cells (HBMECs), reduced apoptosis, reduced Fe2+, IL-1β, and IL-6 levels, restored the JC-1 mitochondrial membrane potential, and increased the expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). Analysis identified six overlapping genes between AS and AD. Gene ontology (GO) functional annotation of these genes showed significant enrichment in response to hypoxia, neuron differentiation, and mitochondrial function. Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis revealed significant enrichment in tumor necrosis factor (TNF) signaling pathway, IL-17 signaling pathway, and others. Molecular docking demonstrated that AS could stably bind to the PPP1CC protein. Further experiments showed that PPP1CC knockdown exerted regulatory effects on Aβ1-42-induced HBMECs similar to those exerted by AS, whereas PPP1CC overexpression produced the opposite effects. CONCLUSION: AS protects Aβ1-42-induced HBMECs, likely through modulating PPP1CC expression.</p>

Zhang P, Xie J, Liu L, Zheng Y, Yang Y, Annals of clinical and laboratory science
In Vitro Study

Inflammation-targeted nanoaggregates encapsulated triptolide and hyperoside for M2 macrophage repolarization and oxidative stress reversal in rheumatoid arthritis therapy.

M1 macrophages are pivotal in rheumatoid arthritis (RA) pathogenesis, accompanied by releasing pro-inflammatory cytokines and reactive oxygen species (ROS). As a traditional anti-RA herbal ingredient, triptolide (TP) exerts potent anti-inflammatory effects via M1 macrophage modulation, but is clinically limited by poor solubility,‌elevating ROS and systemic toxicity. Herein, we synthesized aβ-cyclodextrin-grafted poly-L-glutamic acid copolymer, forming nanoaggregates (NPS) loaded with TP and hyperoside (HYP, a potent antioxidant) via host-guest interactions for RA treatment. The NPS exhibit a suitable particle size (150 nm), excellent stability and high encapsulation efficiency of 93.77% for HYP, and 86.98% for TP. NPS can selectively target M1 macrophages through HYP's galactose residues, exerting strong anti-inflammatory effects via M1-to-M2 macrophage polarization. Thereinto, HYP mitigates both RA-associated and TP-induced oxidative stress by scavenging ROS and activating antioxidant enzymes, achieving a dual effect of anti-inflammation and detoxification. In CIA mice, NPS significantly increased drug accumulation in inflamed joints relative to TP, enhancing the synergistic anti-arthritic efficacy of HYP and TP, while reducing TP-induced hepatic oxidative stress and elevating plantar pain thresholds. Overall, NPS is a promising M1 macrophage-targeted nanoaggregate for precise RA therapy and adverse effect reduction, which may improve clinical translatability of TP.

Zhonghui Xue, Huijie Zhou, Jingru Cui, Yujie Chen, Xiaofang Li, Min Yan, Xiangxiang Wu, Huahui Zeng, Colloids Surf B Biointerfaces
In Vitro Study

Decoding the extracts of Lippia alnifolia Schauer (Verbenaceae): Chemical composition and its impacts on nociception and inflammation.

ETHNOPHARMACOLOGICAL RELEVANCE: Lippia alnifolia Schauer (Verbenaceae) is an aromatic medicinal plant known as "alecrim-de-vaqueiro" and endemic to the Brazilian Caatinga. Its leaves are traditionally used by local populations for the treatment of infections and as a natural antiseptic. AIM OF THE STUDY: This study aimed to perform the first chemical characterization of extracts obtained from the leaves and inflorescences of L. alnifolia, to evaluate their antinociceptive and anti-inflammatory activities, and to investigate the mechanisms underlying these effects. MATERIAL AND METHODS: The chemical composition of extracts and isolated compounds was determined by chromatographic and spectrometric procedures. Experimental animal models were used to evaluate the antinociceptive and anti-inflammatory effects in male mice. Toxicological evaluation was conducted separately in female mice. The extracts were administered orally at doses of 75, 150 and 300 mg/kg, and their effects were compared to both positive and negative controls across all protocols. In selected assays, animals were pre-treated with pharmacological antagonists (naloxone, glutamate and cinnamaldehyde) to explore potential mechanisms. RESULTS: LC-MS/MS analysis revealed the presence of phenolic compounds, iridoids, and phenylpropanoids, and the bioactive compounds jaceosidin and verbascoside were isolated. The extracts showed no signs of acute toxicity and did not impair motor coordination, indicating the absence of central nervous system depression. In the acetic acid-induced writhing test, the leaf and inflorescence extracts reduced the number of writhings by 49.39 ± 7.9 % and 58.24 ± 8.8 %, respectively, compared with the control group. In the formalin test, the leaf extract reduced paw licking time by 55.76 ± 2,8 % (phase I) and 67.52 ± 4,5 % (phase II), while the inflorescence extract produced inhibitions of 54.39 ± 1,9 % (phase I) and 72.56 ± 3,1 % (phase II). In the hot plate test, the leaves and inflorescences extracts produced a significant response in the first 30 min with the highest dose 300 mg/kg (27,3 ± 4,1 s and 25,5 ± 5,7 s, respectively). In the Randall-Selitto test, both extracts increased the mechanical hyperalgesia threshold at all tested doses. In the formalin-induced paw edema model, the highest dose (300 mg/kg) produced significant inhibition of edema at 60, 120, and 180 min. Mechanistic assays indicated that the antinociceptive effects are not mediated by opioid receptors. CONCLUSION: These findings provide experimental support for the ethnopharmacological use of L. alnifolia in conditions associated with inflammation and pain. Although antimicrobial activity was not evaluated, the observed peripheral anti-inflammatory and antinociceptive effects may contribute to symptom relief in infection-related conditions. The differences observed between leaf and inflorescence extracts indicate that plant part selection is a relevant factor in future pharmacological, phytochemical, and standardization studies.

Paulo IMM, Bomfim HF, Silva AN, Perilla ACG, Yamaguchi LF, Kato MJ, Rocha ML, Lucchese AM, Journal of ethnopharmacology

HSYA attenuates Inflammation - Necroptosis to ameliorate secondary brain injury after intracerebral hemorrhage.

ETHNOPHARMACOLOGICAL SIGNIFICANCE: Hydroxysafflor yellow A (HSYA), an active constituent extracted from the traditional Chinese herb safflower (Carthamus tinctorius L.), has been used in stroke therapy for centuries and is well known for its anti-inflammatory and neuroprotective properties. However, the mechanisms through which HSYA mitigates Secondary Brain Injury (SBI) following intracerebral hemorrhage (ICH) remain incompletely understood. AIM OF THE STUDY: This study provides a systematic evaluation of the neuroprotective effects of HSYA against SBI, with a particular focus on elucidating its regulatory role in the necroptosis pathway. MATERIALS AND METHODS: An ICH model was established in Sprague-Dawley (SD) rats via autologous blood injection. The neuroprotective efficacy of HSYA was evaluated using the modified neurological severity score (mNSS), monitoring of body weight, and measurement of brain water content to assess cerebral edema, complemented by histological and molecular analyses (TUNEL, ELISA, immunofluorescence (IF), and Western blot). Molecular dynamics simulation (MD) and molecular docking were performed to characterize the binding properties of HSYA with key necroptosis-related proteins, including phospho-receptor-interacting protein kinase 1(p-RIPK1), phospho-receptor-interacting protein kinase 3(p-RIPK3), and phospho-mixed lineage kinase-like protein(p-MLKL). An in vitro ICH model was generated using hemin-stimulated BV2 cells. The effects of HSYA were examined by assessing cell viability, quantifying inflammatory cytokines (TNF-α, IL-1β, IL-6), and determining the expression of necroptosis-associated proteins and inflammatory mediators (TNF-α, high mobility group box-1(HMGB1)). RESULTS: In vivo, HSYA treatment markedly improved mNSS scores and alleviated neuroinflammation, microglial activation, as well as both apoptotic and necroptotic cell death. MD and molecular docking analyses further demonstrated that HSYA exhibits stable binding to the critical phosphorylation sites of receptor-interacting protein kinase 1(RIPK1), receptor-interacting protein kinase 3(RIPK3), and mixed lineage kinase-like protein (MLKL), primarily through interactions involving its hydroxyl groups and aromatic ring structures. Consistently, in vitro experiments showed that HSYA enhanced BV2 cell viability, reduced the release of pro-inflammatory cytokines, and attenuated both apoptosis and necroptosis in hemin-stimulated BV2 cell. CONCLUSION: HSYA may alleviate neurological dysfunction associated with SBI following ICH, potentially by suppressing microglial activation and modulating the necroptosis pathway, thereby interrupting the "inflammation-necroptosis-secondary inflammation" cascade. These findings provide preliminary experimental evidence supporting HSYA as a promising neuroprotective candidate for the treatment of SBI.

Lei Luo, Qiang Ma, Yuanchen Liao, Mei Xiang, Xiaofeng Gao, Zhong Li, Siyang Yan, Desheng Zhou, Qihou Su, J Ethnopharmacol
Animal Study

Videos (6)

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The Root Cause of Inflammation and Other Modern Diseases
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The Root Cause of Inflammation and Other Modern Diseases

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Video Feed Aug 3, 2014

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Disease Causing Inflammation is Caused by This!
Video Feed Feb 12, 2015

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