scholarly journals Astragaloside IV exerts anti-inflammatory role in endometriosis by downregulating TLR4/NF-κB pathway

2021 ◽  
Vol 18 (3) ◽  
pp. 539-545
Author(s):  
Yongping Zhang ◽  
Ouping Huang ◽  
Wei Zhang ◽  
Luxin Liu ◽  
Caiwei Xu
Keyword(s):  
Inflammatory Cytokines ◽  
Underlying Mechanism ◽  
Nuclear Factor Κb ◽  
Enzyme Linked Immunosorbent Assay ◽  
Astragaloside Iv ◽  
Tnf Α ◽  
Hematoxylin And Eosin ◽  
And Control ◽  
Novel Drug

Purpose: To investigate the effect of astragaloside IV administration on the inflammatory response in endometriosis and the underlying mechanism of action. Methods: Mice were divided into two groups: endometriosis (EMs) mice and control mice (n = 12). EMs induction in mice was achieved by transplantation of mouse uterine tissue. The same procedure was performed in control mice except that a separate suture was inserted instead of endometrial tissue. After 5 weeks, EMs mice were treated with or without astragaloside IV (AIV). The tissue lesions in EMs and control mice were stained with hematoxylin and eosin staining. The activation of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) p65 signaling was evaluated by western blot, while expression of inflammatory cytokines was evaluated by quantitative real-time-polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA). Results: Astragaloside IV repressed the inflammation of murine Ems lesions, and also dampened the activation of TLR4/NF-κB signaling in vivo and vitro (p < 0.01 and p < 0.001, respectively). In addition, the expression levels of inflammatory cytokines (IL-1β, IL-6, Ccl-2, and TNF-α) decreased following AIV treatment in vivo. Conclusion: The results indicate that TLR4/NF-κB signaling pathways are closely related to the inhibition of Ems inflammation by astragaloside IV. Thus, astragaloside IV may be a novel drug for the prevention and treatment of endometrioses.

scholarly journals The secret behind peripheral inflammation and depression: The hypothalamus

2020 ◽  
Author(s):  
Bruno Pedraz Petrozzi ◽  
Carlo Blecker ◽  
Elena Neumann ◽  
Gebhard Sammer
Keyword(s):  
Mixed Models ◽  
Enzyme Linked Immunosorbent Assay ◽  
Resonance Spectroscopy ◽  
Peripheral Inflammation ◽  
Tnf Α ◽  
Ifn Γ ◽  
And Control ◽  
Hpa Axis Activity ◽  
Inflammatory Component

Abstract In recent years there has been increasing evidence of an inflammatory component due to overstimulation of the hypothalamic-pituitary-adrenals (HPA) in depression. The glutamate metabolites (glutamate and glutamine) are important metabolites that are involved in this stimulation. The aim of this study was to determine the concentrations of hypothalamic glutamate metabolites in depression and to investigate their relationship to peripheral inflammation. Participants with diagnosed depression (DE; n = 24) and control subjects without depression (HC; n = 25) were investigated. Hypothalamic glutamate metabolites were recorded using in vivo magnetic resonance spectroscopy. Peripheral cytokines (IL-6, TNF-α, IFN-γ and IL-1β) were assessed using Enzyme-Linked Immunosorbent Assay. For statistical analysis, generalized mixed models were computed using Poisson distributions and a log link function. The results show overall higher hypothalamic glutamate metabolites in DE compared to HC. High TNF-a and IL-1ß concentrations are associated with high hypothalamic glutamate metabolites in DE. These results provide initial evidence that, in depression, increased HPA axis activity is associated with peripheral inflammation favored by hypothalamic glutamate metabolites.

Metallothionein modulates lipopolysaccharide-stimulated tumour necrosis factor expression in mouse peritoneal macrophages

2002 ◽  
Vol 361 (2) ◽  
pp. 363-369 ◽  
Author(s):  
Masako KANEKIYO ◽  
Norio ITOH ◽  
Atsuko KAWASAKI ◽  
Akiko MATSUYAMA ◽  
Kimihiro MATSUDA ◽  
...  
Keyword(s):  
Heavy Metals ◽  
Tumour Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Metal Binding ◽  
Tumour Necrosis ◽  
Nuclear Factor Κb ◽  
Peritoneal Macrophages ◽  
Tnf Α ◽  
Necrosis Factor

Metallothionein (MT) is a low-molecular-mass, cysteine-rich metal binding protein thought to be involved in the detoxification of heavy metals and scavenging of free radicals. MT is directly induced not only by heavy metals, but also by hormones and cytokines. The present study, which uses mice with genetic deletions of the MT proteins (MT−/- mice), was designed to evaluate the effects of MT on the expression of pro-inflammatory cytokines in macrophages. We found that the production of tumour necrosis factor (TNF) induced by lipopolysaccharide (LPS) in peritoneal macrophages is up-regulated by MT via the modulation of nuclear factor κB (NF-κB) activity. This conclusion is supported by the following observations: (1) LPS stimulated the secretion of less TNF activity from MT−/- peritoneal exudate macrophages (PEMs) than from wild-type controls (MT+/+ mice) without a difference in the pattern of kinetics; (2) LPS-stimulated expression of TNF-α mRNA was decreased in MT−/- PEMs; (3) LPS-stimulated activation of NF-κB was decreased in MT−/- PEMs; and (4) production of TNF in PEMs of MT−/- mice after LPS treatment in vivo was decreased (compared with MT+/+ PEMs). Expression of other inflammatory cytokines, interleukin (IL)-1α and IL-6 mRNA, which were modulated by NF-κB, were also down-regulated in MT−/- PEMs. Thus MT plays a key role in the LPS-induced activation of PEMs via the modulation of NF-κB activity.

scholarly journals In vitro and in vivo anti-inflammatory properties of Mayan propolis

2020 ◽  
Vol 18 ◽  
pp. 205873922093528
Author(s):  
Jorge Xool-Tamayo ◽  
Ivan Chan-Zapata ◽  
Víctor Ermilo Arana-Argaez ◽  
Fabiola Villa-de la Torre ◽  
Julio César Torres-Romero ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
High Performance ◽  
Enzyme Linked Immunosorbent Assay ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Main Components ◽  
Macrophage Viability

Introduction Propolis has been used traditionally for different human diseases and even recently as dental biomaterials because of its antibacterial, antimycotic, and anti-inflammatory properties. However, a proper correlation between in vitro and in vivo anti-inflammatory properties has not been clearly established. Methods The composition of propolis was determined by high-performance liquid chromatography–ultraviolet mass spectrometry (HPLC-UV-MS). Viability of ethanolic propolis solution was evaluated by thiazolyl blue tetrazolium bromide (MTT) assay on murine macrophages. The anti-inflammatory properties were assessed both in vitro through the enzyme-linked immunosorbent assay (ELISA) quantification of various cytokines and in vivo by induced edemas. Results Chemical analysis showed pinocembrin, pinobanksin-3-O-acetate, and pinobanksin-3-O-propionate as the main components of propolis. Macrophage viability was high (106%) when propolis was used up to 50 µg/mL. ELISA studies showed a reduction in the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) up to 145 pg/mL, 350 pg/mL, and 210 pg/mL, respectively, while the anti-inflammatory cytokines (IL-10 and IL-4) were increased up to 833 pg/mL and 446 pg/mL. Finally, edema was reduced on paw and ear mice by 9% and 22%, respectively. Conclusion Mayan propolis has strong in vitro anti-inflammatory properties without compromising macrophage viability, resulting in a low-to-mild in vivo anti-inflammatory response.

scholarly journals Hypothalamic Glutamine-Glutamate Metabolites and Peripheral Pro-Inflammatory Cytokines in Participants with Depression: A Case-Control Study

2020 ◽  
Author(s):  
Bruno Pedraz Petrozzi ◽  
Carlo Blecker ◽  
Elena Neumann ◽  
Gebhard Sammer
Keyword(s):  
Enzyme Linked Immunosorbent Assay ◽  
Resonance Spectroscopy ◽  
Peripheral Inflammation ◽  
Tnf Α ◽  
Ifn Γ ◽  
And Control ◽  
Pituitary Adrenal Axis ◽  
Inflammatory Component ◽  
Control Study

Abstract Background: In recent years, there has been increasing evidence of an inflammatory component due to overstimulation of the hypothalamic-pituitary-adrenal axis (HPAA) in depression. The glutamate metabolites (glutamate and glutamine) are important in this stimulation. The aim of this study was to determine the concentrations of hypothalamic glutamate metabolites in depression and to investigate their relationship to peripheral inflammation. Methods: Participants with diagnosed depression (DE; n = 24) and control subjects without depression (HC; n = 25) were investigated. Hypothalamic glutamate metabolites were recorded using in vivo magnetic resonance spectroscopy. Peripheral cytokines (IL-6, TNF-α, IFN-γ and IL-1β) were assessed using Enzyme-Linked Immunosorbent Assay. For statistical analysis, generalized mixed models were computed using Poisson distributions and a log link function. Results: The results show overall higher hypothalamic glutamate metabolites in DE compared to HC. High TNF-α and IL-1β concentrations are associated with high hypothalamic glutamate metabolites in DE. Conclusions: These results provide initial evidence that, in depression, increased HPAA activity is associated with peripheral inflammation favored by hypothalamic glutamate metabolites.

scholarly journals Anti-arthritic effect of total anthraquinone from Polygonum cuspidatum on type II collagen-induced arthritis in rats

2017 ◽  
Vol 16 (10) ◽  
pp. 2453-2459
Author(s):  
Feng Wang ◽  
Yan-hong Qiao ◽  
Hui-min Niu ◽  
Hong Zhao
Keyword(s):  
Inflammatory Cytokines ◽  
Type Ii Collagen ◽  
Serum Levels ◽  
Underlying Mechanism ◽  
Enzyme Linked Immunosorbent Assay ◽  
Type Ii ◽  
Polygonum Cuspidatum ◽  
Collagen Induced Arthritis ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Purpose: To study the anti-arthritic effect of total anthraquinone from Polygonum  cuspidatum (TAPC) on type II collagen-induced arthritis (CIA) in rats, and to  investigate the underlying mechanism(s).Methods: CIA rats were prepared and treated orally with TAPC at doses of 50, 100 and 200 mg/kg/day, for 24 days. Paw volume and arthritis score were measured prior to TAPC treatment, and subsequently at 3-day intervals on days 3, 6, 9, 12, 15, 18, 21 and 24. Serum levels of TNF-α, IL-6 and IL-17 were determined by enzyme-linked immunosorbent assay (ELISA), while synovial tissue TNF-α, IL-6 and IL-17mRNA expressions were assayed by real time-polymerase chain reaction (RT-PCR). Thymus and spleen indices were also determined.Results: TAPC (50, 100 and 200 mg/kg) significantly alleviated paw swelling (p < 0.05), arthritis scores (p < 0.05) and thymus and spleen indices (p < 0.05) of CIA rats, when compared with the control rats. In addition, TAPC significantly decreased serum levels of the pro-inflammatory cytokines TNF-α, IL-6 and IL-17 (p < 0.01); and down-regulated their mRNA expressions in synovial tissues (p < 0.01).Conclusion: These results suggest that TAPC exerts good anti-arthritic activity in rats, most probably via suppression of inflammatory responses.Keywords: Polygonum cuspidatum, Anthraquinone, Type II collagen-induced  arthritis, Pro-inflammatory cytokines

scholarly journals microRNA-27b shuttled by mesenchymal stem cell-derived exosomes prevents sepsis by targeting JMJD3 and downregulating NF-κB signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jia Sun ◽  
Xuan Sun ◽  
Junhui Chen ◽  
Xin Liao ◽  
Yixuan He ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Cecal Ligation ◽  
Gene Promoter ◽  
In Silico Analysis ◽  
Underlying Mechanism ◽  
Nuclear Factor Κb ◽  
Pro Inflammatory Cytokines

Abstract Background Exosomal microRNAs (miRs) derived from mesenchymal stem cells (MSCs) have been shown to play roles in the pathophysiological processes of sepsis. Moreover, miR-27b is highly enriched in MSC-derived exosomes. Herein, we aimed to investigate the potential role and downstream molecular mechanism of exosomal miR-27b in sepsis. Methods Inflammation was induced in bone marrow-derived macrophages (BMDMs) by lipopolysaccharide (LPS), and mice were made septic by cecal ligation and puncture (CLP). The expression pattern of miR-27b in MSC-derived exosomes was characterized using RT-qPCR, and its downstream gene was predicted by in silico analysis. The binding affinity between miR-27b, Jumonji D3 (JMJD3), or nuclear factor κB (NF-κB) was characterized to identify the underlying mechanism. We induced miR-27b overexpression or downregulation, along with silencing of JMJD3 or NF-κB to examine their effects on sepsis. The production of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 was detected by ELISA. Results miR-27b was highly expressed in MSC-derived exosomes. Mechanistic investigations showed that miR-27b targeted JMJD3. miR-27b decreased expression of pro-inflammatory genes by inhibiting the recruitment of JMJD3 and NF-κB at gene promoter region. Through this, MSC-derived exosomal miR-27b diminished production of pro-inflammatory cytokines in LPS-treated BMDMs and septic mice, which could be rescued by upregulation of JMJD3 and NF-κB. Besides, in vitro findings were reproduced by in vivo findings. Conclusion These data demonstrated that exosomal miR-27b derived from MSCs inhibited the development of sepsis by downregulating JMJD3 and inactivating the NF-κB signaling pathway.

scholarly journals Pirfenidone attenuates synovial fibrosis and postpones the progression of osteoarthritis by anti-fibrotic and anti-inflammatory properties in vivo and in vitro

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qilu Wei ◽  
Ning Kong ◽  
Xiaohui Liu ◽  
Run Tian ◽  
Ming Jiao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Fast Green ◽  
Expression Levels ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Safranin O ◽  
Tgf Β1

Abstract Background Osteoarthritis (OA) is a disease of the entire joint involving synovial fibrosis and inflammation. Pathological changes to the synovium can accelerate the progression of OA. Pirfenidone (PFD) is a potent anti-fibrotic drug with additional anti-inflammatory properties. However, the influence of PFD on OA is unknown. Methods Proliferation of human fibroblast-like synoviocytes (FLSs) after treatment with TGF-β1 or PFD was evaluated using a Cell Counting Kit-8 assay and their migration using a Transwell assay. The expression of fibrosis-related genes (COL1A1, TIMP-1, and ACTA-2) and those related to inflammation (IL-6 and TNF-α) was quantified by real-time quantitative PCR. The protein expression levels of COL1A1, α-SMA (coded by ACTA-2), IL-6 and TNF-α were measured by enzyme-linked immunosorbent assay. A rabbit model of OA was established and then PFD was administered by gavage. The expression of genes related to fibrosis (COL1A1, TIMP-1, and ADAM-12) and inflammation (IL-6 and TNF-α) was measured using RNA extracted from the synovium. Synovial tissue was examined histologically after staining with H&E, Masson’s trichrome, and immunofluorescence. Synovitis scores, the volume fraction of collagen, and mean fluorescence intensity were calculated. Degeneration of articular cartilage was analyzed using a Safranin O-fast green stain and OARSI grading. Results The proliferation of FLSs was greatest when induced with 2.5 ng/ml TGF-β1 although it did not promote their migration. Therefore, 2.5 ng/ml TGF-β1 was used to stimulate the FLSs and evaluate the effects of PFD, which inhibited the migration of FLSs at concentrations as low as 1.0 mg/ml. PFD decreased the expression of COL1A1 while TGF-β1 increased both mRNA and protein expression levels of IL-6 but had no effect on α-SMA or TNF-α expression. PFD decreased mRNA expression levels of COL1A1, IL-6, and TNF-α in vivo. H&E staining and synovitis scores indicated that PFD reduced synovial inflammation, while Masson’s trichrome and immunofluorescence staining suggested that PFD decreased synovial fibrosis. Safranin O-Fast Green staining and the OARSI scores demonstrated that PFD delayed the progression of OA. Conclusions PFD attenuated synovial fibrosis and inflammation, and postponed the progression of osteoarthritis in a modified Hulth model of OA in rabbits, which was related to its anti-fibrotic and anti-inflammatory properties.

scholarly journals Inflammatory cytokines-stimulated human muscle stem cells ameliorate ulcerative colitis via the IDO-TSG6 axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shengchao Zhang ◽  
Jiankai Fang ◽  
Zhanhong Liu ◽  
Pengbo Hou ◽  
Lijuan Cao ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
Human Muscle ◽  
Enzyme Linked Immunosorbent Assay ◽  
Muscle Stem Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory

Abstract Background Muscle stem cells (MuSCs) are absolutely required for the formation, repair, and regeneration of skeletal muscle tissue. Increasing evidence demonstrated that tissue stem cells, especially mesenchymal stem cells (MSCs), can exert therapeutic effects on various degenerative and inflammatory disorders based on their immunoregulatory properties. Human mesenchymal stem cells (hMSCs) treated with interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) were reported to possess anti-inflammatory functions by producing TNF-stimulated gene 6 (TSG-6). However, whether human muscle stem cells (hMuSCs) also possess TSG-6 mediated anti-inflammatory functions has not been explored. Methods The ulcerative colitis mouse model was established by subjecting mice to dextran sulfate sodium (DSS) in drinking water for 7 days. hMuSCs were pretreated with IFN-γ and TNF-α for 48 h and were then transplanted intravenously at day 2 of DSS administration. Body weights were monitored daily. Indoleamine 2,3-dioxygenase (IDO) and TSG-6 in hMuSCs were knocked down with short hairpin RNA (shRNA) and small interfering RNA (siRNA), respectively. Colon tissues were collected for length measurement and histopathological examination. The serum level of IL-6 in mice was measured by enzyme-linked immunosorbent assay (ELISA). Real-time PCR and Western blot analysis were performed to evaluate gene expression. Results hMuSCs treated with inflammatory factors significantly ameliorated inflammatory bowel disease (IBD) symptoms. IDO and TSG-6 were greatly upregulated and required for the beneficial effects of hMuSCs on IBD. Mechanistically, the tryptophan metabolites, kynurenine (KYN) or kynurenic acid (KYNA) produced by IDO, augmented the expression of TSG-6 through activating their common receptor aryl hydrocarbon receptor (AHR). Conclusion Inflammatory cytokines-treated hMuSCs can alleviate DSS-induced colitis through IDO-mediated TSG-6 production.

scholarly journals POS1290 CYTOKINE BIOMARKERS IN COMMON LOW BACK PAIN

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 926.3-926
Author(s):  
R. Dhahri ◽  
A. Dghaies ◽  
M. Slouma ◽  
L. Metoui ◽  
I. Gharsallah ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Low Back Pain ◽  
Back Pain ◽  
Inflammatory Cytokines ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Controls ◽  
Low Back ◽  
Tnf Α ◽  
Functional Scores ◽  
The Mean

Background:Common low back pain (LBP) is a common health problem affecting 50 to 80% of working age adults. It is one of the common and costly health problems in Tunisia. Actually, the role of the immune response and inflammatory cytokines in the pathogenesis of chronic pain has been of growing interest.Objectives:The aim of this study was to assess whether pro and anti-inflammatory cytokines could be detected in serum in patients with LBP compared with healthy subjects and whether they could be related to pain severity and to clinical findings.Methods:It was a an analytical cross-sectional study including 50 patients with at least three months of LBP, in the department of rheumatology, orthopedics and immunology at the Military Hospital of Tunis between January 1st and March 31, 2020. All patients had a standardized clinical assessment.Levels of serum cytokines IL-6, IL-8, IL-1β and TNF- α, were measured using the chimiluminescence technique. Serum concentration of IL-10 was assayed by the enzyme-linked immunosorbent assay technique (ELISA). The normal levels of cytokines were determined in 50 healthy controls.Results:The mean age of the patients was 41.9 ± 8.4 years and the sex ratio was 4.5. LBP duration was 66.4 months. The mean lumbar visual analog scale (VAS) was 4.5 ± 1.9, and the root VAS was 2.6 ± 2.5. Neuropathic pain was found in 26% of patients. The average BMI was 27 ± 3.7 kg/m2. Only serum level of IL-8 was significantly higher in subjects with LBP compared to healthy controls (p <10-3). IL-1β was indetectable in both patients and controls. Positive correlations were found between IL-8 levels and anxiety/functional scores (r = 0.3; p = 0.02/ r = 0.3; p = 0.04). IL-6 was positively correlated with BMI, and negatively correlated with the Schober test. No correlations were found between serum levels of IL-6, IL-8, IL-10, TNF-α and pain intensity (VAS), neuropathic pain (DN4), fibromyalgia (FIRST), depression (HAD) and various radiological data.Conclusion:Interleukin-8 is a biomarker of common low back pain and correlate with anxiety and functional disability. These results suggest that IL-8 may be a therapeutic target to reduce chronic back pain and reduce the social and profession impact.Disclosure of Interests:None declared

Long Noncoding RNA SNHG1 Promotes Lipopolysaccharide-Induced Activation and Inflammation in Microglia via Targeting miR-181b

2021 ◽  
pp. 1-11
Author(s):  
Jun Dong ◽  
Tingkai Fu ◽  
Yunxue Yang ◽  
Zhenxin Mu ◽  
Xingang Li
Keyword(s):  
Inflammatory Cytokines ◽  
Long Noncoding Rna ◽  
Calcium Binding ◽  
Noncoding Rna ◽  
Morphological Changes ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammation Response ◽  
Tnf Α ◽  
Cox 2

<b><i>Introduction:</i></b> Long noncoding RNA small nuclear host gene 1 (SNHG1) was involved in neuroinflammation in microglial BV-2 cells; however, its interaction with microRNA (miR)-181b in lipopolysaccharide (LPS)-induced BV-2 cells remained poor. <b><i>Methods:</i></b> BV-2 cells were treated with LPS and then were subjected to observation on morphology and immunofluorescence staining. After transfection, levels of inflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were determined with enzyme-linked immunosorbent assay (ELISA). The potential binding sites between SNHG1 and miR-181b were confirmed using dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction and Western blot were applied for detecting the mRNA and protein expressions of proinflammatory cytokines, ionized calcium-binding adapter molecule 1 (Iba1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). <b><i>Results:</i></b> LPS led to the morphological changes and activation of BV-2 cells. The transfection of SNHG1 overexpression vector further promoted LPS-induced SNHG1 upregulation, inflammatory cytokines (IL-1β, IL-6, and TNF-α) generation and Iba-1, COX-2, and iNOS expressions, whereas silencing SNHG1 did the opposite. miR-181b functions as a downstream miRNA of SNHG1. In LPS-treated cells, the inhibition of miR-181b induced by SNHG1 promoted inflammation response and the expressions of Iba-1, COX-2, and iNOS. <b><i>Conclusion:</i></b> SNHG1 was involved in LPS-induced microglial activation and inflammation response via targeting miR-181b, providing another evidence of the roles of SNHG1 implicated in neuroinflammation of microglia.

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