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1.
Exp Neurol ; : 113752, 2021 May 08.
Artigo em Inglês | MEDLINE | ID: mdl-33974879

RESUMO

Autophagy is a crucial pathological process in early brain injury (EBI) after subarachnoid hemorrhage (SAH). In this study, we investigated the role of dihydrolipoic acid (DHLA) on enhancing autophagy and alleviating neurological deficits after SAH. SAH was induced by endovascular perforation in male Sprague-Dawley rats. DHLA (30 mg/kg) was administered intraperitoneally 1 h (h) after SAH. Small interfering ribonucleic acid (siRNA) for lysosome-associated membrane protein-1 (LAMP1) was administered through intracerebroventricular (i.c.v) route 48 h before SAH induction. SAH grading score, neurological score, immunofluorescence staining, Fluoro-Jade C (FJC) staining, and Western blot were examined. DHLA treatment increased autophagy-related protein expression and downregulated the apoptosis-related protein expression 24 h after SAH. In addition, the DHLA treatment reduced neuronal cell death and alleviated neurological deficits after SAH. Furthermore, knockdown of LAMP1 abolished the neuroprotective effects of DHLA. These results indicate that LAMP1 may participate in autophagy after SAH. DHLA treatment can enhance autophagy, attenuate apoptosis, and alleviate neurofunctional deficits in EBI after SAH. It may provide an effective alternative method for the treatment of EBI after SAH.

2.
Front Immunol ; 12: 582594, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33815356

RESUMO

Objective: Pediatric diffuse gliomas (pDGs) are relatively rare and molecularly distinct from pediatric pilocytic astrocytoma and adult DGs. Immunotherapy is a promising therapeutic strategy, requiring a deep understanding of tumor immune profiles. The spatial locations of brain tumors might be related to the molecular profiles. We aimed to analyze the relationship between the immune checkpoint molecules with the locations of DGs comparing pediatric with adult patients. Method: We studied 20 pDGs patients (age ≤ 21 years old), and 20 paired adult patients according to gender and histological types selected from 641 adult patients with DGs. Immune checkpoint molecules including B7-H3, CD47, and PD-L1, as well as tumor-infiltrating lymphocytes (TILs) and tumor-associated macrophages (TAMs), were manifested by immunohistochemical staining. Expression difference analyses and Spearman's correlation were performed. MRI data were voxel-wise normalized, segmented, and analyzed by Fisher's exact test to construct the tumor frequency and p value heatmaps. Survival analyses were conducted by Log-rank tests. Result: The median age of pediatric patients was 16 years. 55% and 30% of patients were WHO II and III grades, respectively. The left frontal lobe and right cerebellum were the statistically significant locations for pDGs, while the anterior horn of ventricles for adult DGs. A potential association between the expression of PD-L1 and TAMs was found in pDGs (p = 0.002, R = 0.670). The right posterior external capsule and the lateral side of the anterior horn of the left ventricle were predominant locations for the adult patients with high expression of B7-H3 and low expression of PD-L1 compared to pediatric ones, respectively. Pediatric patients showed significantly improved overall survival compared with adults. The prognostic roles of immune checkpoint molecules and TILs/TAMs were not significantly different between the two groups. Conclusion: Immune checkpoint-associated locations of diffuse gliomas comparing pediatric with adult patients could be helpful for the immunotherapy decisions and design of clinical trials.

4.
Biosens Bioelectron ; 183: 113200, 2021 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-33819904

RESUMO

In this study, we firstly propose a novel smartphone-assisted visualization SNP genotyping method termed competitive activation cross amplification (CACA). The mutation detection strategy depends on the ingenious design of both a start primer and a verification probe with ribonucleotide insertion through competitive combination and perfect matching with the target DNA, Meanwhile, the RNase H2 enzyme was utilized to specifically cleave ribonucleotide insertion and achieve extremely specific dual verification. Simultaneously, the results allow both colorimetric and fluorescence product dual-mode visualization by using self-designed 3D-printed dual function cassette. We validated this novel CACA by analyzing the Salmonella Pullorum rfbS gene at the 237th site, successfully solve the current bottleneck of specific identification and visual detection of this pathogen. The concentration detection limits of the plasmid and genomic DNA were 1500 copies/µL and 3.98 pg/µL, respectively, and as low as the presence of 0.1% mutant-type can be distinguished from 99.9% wild-type. Combined with a powerful hand-warmer, which can provide heating more than 60 °C for 20 h to realize power-free, dual function cassette and smartphone quantitation, our novel CACA platform firstly realizes user-friendly, cost-effective, portable, rapid, and accurate POC detection of SNP.

5.
BMC Neurosci ; 22(1): 15, 2021 Mar 09.
Artigo em Inglês | MEDLINE | ID: mdl-33750300

RESUMO

BACKGROUND: Rupture of intracranial aneurysm (IA) is the main cause of devastating subarachnoid hemorrhage, which urges our understanding of the pathogenesis and regulatory mechanisms of IA. However, the regulatory roles of long non-coding RNAs (lncRNAs) in IA is less known. RESULTS: We processed the raw SRR files of 12 superficial temporal artery (STA) samples and 6 IA samples to count files. Then the differentially expressed (DE) mRNAs, miRNAs, and lncRNAs between STAs and IAs were identified. The enrichment analyses were performed using DEmRNAs. Next, a lncRNA-miRNA-mRNA regulatory network was constructed using integrated bioinformatics analysis. In summary, 341 DElncRNAs, 234 DEmiRNAs, and 2914 DEmRNAs between the STA and IA. The lncRNA-miRNA-mRNA regulatory network of IA contains 91 nodes and 146 edges. The subnetwork of hub lncRNA PVT1 was extracted. The expression level of PVT1 was positively correlated with a majority of the mRNAs in its subnetwork. Moreover, we found that several mRNAs (CCND1, HIF1A, E2F1, CDKN1A, VEGFA, COL1A1 and COL5A2) in the PVT1 subnetwork served as essential components in the PI3K-Akt signaling pathway, and that some of the non-coding RNAs (ncRNAs) (PVT1, HOTAIR, hsa-miR-17, hsa-miR-142, hsa-miR-383 and hsa-miR-193b) interacted with these mRNAs. CONCLUSION: Our annotations noting ncRNA's role in the pathway may uncover novel regulatory mechanisms of ncRNAs and mRNAs in IA. These findings provide significant insights into the lncRNA regulatory network in IA.

6.
Biomed Pharmacother ; 137: 111416, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33761620

RESUMO

RNA modification is an important form of regulation in cancer biology, that is capable of affecting cell proliferation, migration, other genetic characteristics of tumors, and protein expression. Recent research has shown that dysregulation of RNA modification plays an important role in glioma pathogenesis. A key form of RNA post-transcriptional modification, alternative polyadenylation (APA), may represent a mechanism by which genes escape miRNA-mediated inhibition of cancer. Global shortening of 3' untranslated region (3'-UTR)-mediated APA events have become a potential novel marker of cancer progression. Current treatments in which a single gene or pathway is targeted do not have significant therapeutic benefits for glioma patients, while strategies that are less targeted, in which inhibitors of major regulatory hubs such as APA regulators are utilized, may have superior therapeutic effects. However, the precise mechanisms by which untranslated region-alternative polyadenylation (UTR-APA) regulates glioma are poorly understood. In the present review, we will discuss the important roles of UTR-APA in glioma. In addition to the role of APA in the progression of glioma, we will also explore potential treatment options that target these processes to improve the prognosis of glioma patients.

8.
Nanotechnology ; 32(29)2021 Apr 27.
Artigo em Inglês | MEDLINE | ID: mdl-33780911

RESUMO

Polymer nanostructures have drawn tremendous attention due to their wide applications in nanotechnology. However, the morphology of the polymer nanostructures is fragile under harsh conditions such as high-power irradiation and organic-solution environments during the fabrication or the measurement processes, significantly limiting their potential applications. In this work, we propose and demonstrate a simple approach to improve the stability of polymer nanostructures by coating a conformal ultrathin oxide film via atomic-layer deposition. Due to the refractory and dense coating of the oxide layer, the stability of polymer structures is enhanced by the prohibition of deformation occurrences from thermally induced reflow and organic solution. As a proof of concept, poly(methyl methacrylate) (PMMA) nanostructures coated with a sub-10-nm TiO2layer are demonstrated, and the structures exhibit high temperature stability at 180 °C and good resistance to soluble damage from organic solutions. Subsequently, the mechanism of the improved thermal stability is analyzed via mechanical simulations. Such an effective approach is proposed to significantly broaden the application of polymer nanostructures as functional elements for optical structures/devices that require excellent thermal and chemical stability.

9.
Exp Neurol ; 340: 113684, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33676918

RESUMO

Stroke is a leading cause of mortality and morbidity worldwide. Understanding the underlying mechanisms is important for developing effective therapies for treating stroke. Autophagy is a self-eating cellular catabolic pathway, which plays a crucial homeostatic role in the regulation of cell survival. Increasing evidence shows that autophagy, observed in various cell types, plays a critical role in brain pathology after ischemic stroke. Therefore, the regulation of autophagy can be a potential target for ischemic stroke treatment. In the present review, we summarize the recent progress that research has made regarding autophagy and ischemic stroke, including common signaling pathways, the role of autophagic subtypes (e.g. mitophagy, pexophagy, aggrephagy, endoplasmic reticulum-phagy, and lipophagy) in ischemic stroke, as well as the current methods for autophagy detection and potential therapeutic strategy.

10.
Sci Rep ; 11(1): 5773, 2021 Mar 11.
Artigo em Inglês | MEDLINE | ID: mdl-33707584

RESUMO

Dwarf bunt of wheat, which is caused by Tilletia controversa J.G. Kühn, is a soil-borne disease which may lead up to an 80% loss of yield together with degradation of the quality of the wheat flour by production of a fishy smell. In this study, high-throughput sequencing technology was employed to characterize the microbial composition of wheat tissues (roots, spikes, first stem under the ear, and stem base) and rhizosphere soil of wheat varieties that are resistant and susceptible to T. controversa. We observed that the soil fungal community abundance and diversity were higher in resistant varieties than in susceptible varieties in both inoculated and uninoculated wheat, and the abundances of Sordariomycetes and Mortierellomycetes increased in the resistant varieties infected with T. controversa, while the abundances of Dothideomycetes and Bacteroidia increased in the susceptible varieties. Regarding the bacteria present in wheat tissues, the abundances of Chloroflexi, Bacteroidetes, Gemmatimonadetes, Verrucomicrobia and Acidobacteria in the ear and the first stem under the ear were higher than those in other tissues. Our results indicated that the abundances of Sordariomycetes, Mortierellomycetes, Leotiomycetes, Chryseobacterium and Massilia were higher in T. controversa-infected resistant varieties than in their controls, that Dothideomycetes, Bacteroidia, Nocardioides and Pseudomonas showed higher abundances in T. controversa-infected susceptible varieties, and that Curtobacterium, Exiguobacterium, Planococcus, and Pantoea may have higher abundances in both T. controversa-infected susceptible and resistant varieties than in their own controls.

11.
Nanoscale ; 13(9): 5033-5044, 2021 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-33646222

RESUMO

The construction of anode materials for sodium-ion batteries (SIBs) and potassium-ion batteries (PIBs) with a high energy and a long lifespan is significant and still challenging. Here, sulfur-defective vanadium sulfide/carbon fiber composites (D-V5S8/CNFs) are designed and fabricated by a facile electrospinning method, followed by sulfuration treatment. The unique architecture, in which V5S8 nanoparticles are confined inside the carbon fiber, provides a short-range channel and abundant adsorption sites for ion storage. Moreover, enlarged interlayer spacings could also alleviate the volume changes, and offer small vdW interactions and ionic diffusion resistance to store more Na and K ions reversibly and simultaneously. The DFT calculations further demonstrate that sulfur defects can effectively facilitate the adsorption behavior of Na+ and K+ and offer low energy barriers for ion intercalation. Taking advantage of the functional integration of these merits, the D-V5S8/CNF anode exhibits excellent storage performance and long-term cycling stability. It reveals a high capacity of 462 mA h g-1 at a current density of 0.2 A g-1 in SIBs, while it is 350 mA h g-1 at 0.1 A g-1 in PIBs, as well as admirable long-term cycling characteristics (190 mA h g-1/17 000 cycles/5 A g-1 for SIBs and 165 mA h g-1/3000 cycles/1 A g-1 for PIBs). Practically, full SIBs upon pairing with a Na3V2(PO4)3 cathode also exhibit superior performance.

12.
Artigo em Inglês | MEDLINE | ID: mdl-33684897

RESUMO

Two dimensional heterostructures formed by stacking layered materials play an significant role in condensed matter physics and materials science due to their potential applications in high-efficiency nanoelectronic and optoelectronic devices. In this paper, the structure along with the electronic and optical characteristics of the SiC/CrS2 van der Waals heterostructure (vdWHs) have been investigated by means of density functional theory calculations. It is confirmed that the SiC/CrS2 vdWHs is energetically and thermodynamically stable indicating its great promise for experimental realization. We find that the SiC/CrS2 vdWHs has a direct-band gap and type-II (staggered) band alignment, which can effectively separate the photo-induced electrons and holes pairs and extend their life time. The carrier mobilities of electrons and holes along the armchair and zigzag directions are as high as 6.621×103 and 6.182×104 cm2/V⋅s, respectively. Besides, the charge difference and potential drop across the interface can induce a large built-in electric field across the heterojunction, which will further hinder the electron and hole recombination. The SiC/CrS2 vdWHs has enhanced optical absorption capability compared to individual monolayers. This study demonstrates that the SiC/CrS2 vdWHs is a good candidate for application in the nanoelectronic and optoelectronic devices.

13.
Cell Commun Signal ; 19(1): 40, 2021 Mar 24.
Artigo em Inglês | MEDLINE | ID: mdl-33761934

RESUMO

BACKGROUND: Lysosome-associated membrane protein type 2A (LAMP-2A) is the key component of chaperone-mediated autophagy (CMA), a cargo-selective lysosomal degradation pathway. Aberrant LAMP-2A expression and CMA activation have been demonstrated in various human malignancies. The study focusing on the intrinsic role of LAMP-2A and CMA in glioblastoma (GBM), and downstream mechanism could provide valuable insight into the pathogenesis and novel therapeutic modality of GBM. METHODS: The levels of LAMP-2A, nuclear receptor co-repressor (N-CoR), unfolded protein response (UPR) and apoptosis were examined in clinical samples. LAMP-2A siRNA and shRNA were constructed to manipulate CMA activation. The role of CMA and downstream mechanism through degradation of N-CoR and arresting UPR mediated apoptosis were explored in GBM cells and nude mouse xenograft model. RESULTS: Elevated LAMP-2A and associated decreased N-CoR expression were observed in GBM as compared with peritumoral region and low-grade glioma. Inhibited UPR and apoptosis were observed in GBM with high LAMP-2A expression. In vitro study demonstrated co-localization and interaction between LAMP-2A and N-CoR. LAMP-2A silencing up-regulated N-CoR and aroused UPR pathway, leading to apoptosis, while N-CoR silencing led to an opposite result. In vivo study further confirmed that LAMP-2A inhibition arrested tumor growth by promoting apoptosis. CONCLUSIONS: Our results demonstrated the central role of CMA in mediating N-CoR degradation and protecting GBM cells against UPR and apoptosis, and provided evidence of LAMP-2A as potential biomarker. Further research focusing on CMA with other tumorigenic process is needed and selective modulators of LAMP-2A remain to be investigated to provide a novel therapeutic strategy for GBM. Video Abstract.

14.
Oxid Med Cell Longev ; 2021: 6659282, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33777317

RESUMO

Melatonin is a strong antioxidant which beneficially protects against middle cerebral artery occlusion (MCAO) followed by hemorrhagic transformation in rats; protection includes the reduction of neurological deficits, infarction, and hematoma volume. The molecular mechanisms underlying these neuroprotective effects in the MCAO model have not been clearly identified. This study examined the influence and involved mechanism of melatonin on inflammation in hemorrhagic transformation following hyperglycemia MCAO rat model. Compared with the MCAO group, MCAO+dextrose (DX) group showed worse neurological function and higher infarction and hematoma volume. Interestingly, the protein expression of Nod-like receptor protein 3 (NLRP3) inflammasome increased in the MCAO+DX group compared with the MCAO group, which indicated that NLRP3 inflammasome may be involved in the DX-induced hemorrhagic transformation following MCAO. Then, three dosages of melatonin were intraperitoneally injected 2 h after MCAO induction. Melatonin treatment attenuated inflammatory response by inhibiting the reactive oxygen species (ROS) and NLRP3 inflammasome, alleviating neuronal injury, and reducing infarction and hematoma volume, finally improving neurological score. Melatonin also repressed cortical levels of proinflammatory cytokine IL-1ß, which were increased 24 h after hyperglycemia MCAO. In order to identify the potential mechanisms, we further revealed that nigericin administration reversed the neuroprotective effect of melatonin by promoting NLRP3 inflammasome activation. In general, this present study reveals that melatonin prevents the occurrence of hyperglycemia-enhanced hemorrhagic transformation, and this effect might be beneficial to attenuate neurological dysfunction via suppressing the inflammatory response after MCAO which possibly associated with the inhibition of the ROS/NLRP3 inflammasome pathway.

15.
Front Immunol ; 12: 617163, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33659003

RESUMO

Preclinical and clinical research has demonstrated that inflammation is a critical factor regulating intracerebral hemorrhage (ICH)-induced brain injury. Growing evidence suggests that myeloid cells and lymphocytes have an effect on the pathophysiological processes associated with ICH, such as inflammation, immune responses, perihematomal edema formation, blood-brain barrier (BBB) integrity, and cell death. However, the underlying mechanisms remain largely unknown. We aimed to explore the role immune cells played at different stages of the ICH. To achieve this, novel bioinformatics algorithms were employed to analyze the gene expression profiles and three different analytical tools were utilized to predict the abundances of cell types. In this study, we found that natural killer (NK) cells infiltrated into the brain parenchyma after ICH. Infiltrating NK cells may mediate brain injury through degranulation and recruitment of other cells. Besides, in the acute phase of ICH, monocytes in peripheral blood carried out phagocytosis and secretion of cytokines. On the other hand, in the subacute stage, non-classical monocytes were activated and showed a stronger ability to carry out heme metabolism, wound healing, and antigen processing and presentation. In conclusion, our findings emphasize the significance of intracerebral infiltrating immunocytes in ICH and demonstrate that ICH is a systemic disease affected by peripheral blood. The hub genes identified might be promising therapeutic targets. We also provide a reference on how to use bioinformatics approaches to explore non-neoplastic immune-related diseases.

16.
Sci Adv ; 7(1)2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33523857

RESUMO

In ultraviolet (UV) radiation-exposed skin, mutations fuel clonal cell growth. The relationship between UV exposure and the accumulation of clonal mutations (CMs) and the correlation between CMs and skin cancer risk are largely unexplored. We characterized 450 individual-matched sun-exposed (SE) and non-SE (NE) normal human skin samples. The number and relative contribution of CMs were significantly different between SE and NE areas. Furthermore, we identified hotspots in TP53, NOTCH1, and GRM3 where mutations were significantly associated with UV exposure. In the normal skin from patients with cutaneous squamous cell carcinoma, we found that the cancer burden was associated with the UV-induced mutations, with the difference mostly conferred by the low-frequency CMs. These findings provide previously unknown information on UV's carcinogenic effect and pave the road for future development of quantitative assessment of subclinical UV damage and skin cancer risk.

17.
Poult Sci ; 100(2): 1059-1067, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33518064

RESUMO

Salmonella enterica serovar Gallinarum biovars Pullorum (S. Pullorum) is an infectious bacterial pathogen in the poultry industry that causes systemic pullorum disease. This disease causes great losses in terms of the clinical production and quality of chicken products in breeding farms. However, an acknowledged usable rapid detection method for its specific identification has not been reported, and it is generally difficult to distinguish from fowl typhoid caused by Salmonella enterica serovar Gallinarum biovars Gallinarum. The development of a specific and rapid detection method for this pathogen is therefore needed. In the present study, we targeted the single-nucleotide mutation position 237 of the S. Pullorum rfbS gene to develop an enzyme-activated blocked probe for its clinical rapid detection. The method displayed robust specificity and reproducibility, and it achieved minimal detection limits of 21 copies/µL of copy number and 4.53 pg/µL of genomic DNA. Compared with traditional identification and PCR methods, this method performed better for the detection of 100 clinical actual samples and without false negative results. The entire process can be accomplished in a 1-step closed-tube operation, overcomes the difficulties currently associated with S. Pullorum detection, and provides a specific and rapid method with broad application potential for SNP detection.


Assuntos
Galinhas , Doenças das Aves Domésticas/diagnóstico , Salmonelose Animal/diagnóstico , Salmonella enterica/isolamento & purificação , Animais , Doenças das Aves Domésticas/microbiologia , Reprodutibilidade dos Testes , Salmonella enterica/classificação , Salmonella enterica/genética , Fatores de Tempo
18.
J Neuroinflammation ; 18(1): 43, 2021 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-33588866

RESUMO

BACKGROUND: Intracerebral hemorrhage (ICH) can induce excessive accumulation of reactive oxygen species (ROS) that may subsequently cause severe white matter injury. The process of oligodendrocyte progenitor cell (OPC) differentiation is orchestrated by microglia and astrocytes, and ROS also drives the activation of microglia and astrocytes. In light of the potent ROS scavenging capacity of ceria nanoparticles (CeNP), we aimed to investigate whether treatment with CeNP ameliorates white matter injury by modulating ROS-induced microglial polarization and astrocyte alteration. METHODS: ICH was induced in vivo by collagenase VII injection. Mice were administered with PLX3397 for depleting microglia. Primary microglia and astrocytes were used for in vitro experiments. Transmission electron microscopy analysis and immunostaining were performed to verify the positive effects of CeNP in remyelination and OPC differentiation. Flow cytometry, real-time polymerase chain reaction, immunofluorescence and western blotting were used to detect microglia polarization, astrocyte alteration, and the underlying molecular mechanisms. RESULTS: CeNP treatment strongly inhibited ROS-induced NF-κB p65 translocation in both microglia and astrocytes, and significantly decreased the expression of M1 microglia and A1 astrocyte. Furthermore, we found that CeNP treatment promoted remyelination and OPC differentiation after ICH, and such effects were alleviated after microglial depletion. Interestingly, we also found that the number of mature oligodendrocytes was moderately increased in ICH + CeNP + PLX3397-treated mice compared to the ICH + vehicle + PLX3397 group. Therefore, astrocytes might participate in the pathophysiological process. The subsequent phagocytosis assay indicated that A1 astrocyte highly expressed C3, which could bind with microglia C3aR and hinder microglial engulfment of myelin debris. This result further replenished the feedback mechanism from astrocytes to microglia. CONCLUSION: The present study reveals a new mechanism in white matter injury after ICH: ICH induces M1 microglia and A1 astrocyte through ROS-induced NF-κB p65 translocation that hinders OPC maturation. Subsequently, A1 astrocytes inhibit microglial phagocytosis of myelin debris via an astrocytic C3-microglial C3aR axis. Polyethylene glycol-CeNP treatment inhibits this pathological process and ultimately promotes remyelination. Such findings enlighten us that astrocytes and microglia should be regarded as a functional unit in future works.

19.
Am J Chin Med ; 49(2): 413-435, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33622215

RESUMO

The intestinal tract plays an essential role in protecting tissues from the invasion of external harmful substances due to impaired barrier function. Furthermore, it participates in immunomodulation by intestinal microorganisms, which is important in health. When the intestinal tract is destroyed, it can lose its protective function, resulting in multiple systemic complications. In severe cases, it may lead to systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). Thus far, there are no curative therapies for intestinal mucosal barrier injury, other than a few drugs that can relieve symptoms. Thus, the development of novel curative agents for gastrointestinal diseases remains a challenge. Ursolic acid (UA) and its isomer, Oleanolic acid (OA), are pentacyclic triterpene acid compounds. Both their aglycone and glycoside forms have anti-oxidative, anti-inflammatory, anti-ulcer, antibacterial, antiviral, antihypertensive, anti-obesity, anticancer, antidiabetic, cardio protective, hepatoprotective, and anti-neurodegenerative properties in living organisms. In recent years, several studies have shown that UA and OA can reduce the risk of intestinal pathological injury, alleviate intestinal dysfunction, and restore intestinal barrier function. The present study evaluated the beneficial effects of UA and OA on intestinal damage and diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC).

20.
J Clin Immunol ; 41(3): 565-575, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33392854

RESUMO

SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) syndrome shows a wide variability in musculoskeletal and cutaneous manifestations, and it is therefore underrecognized and misdiagnosed in the clinic due to a lack of specific markers. In this study, we aimed to identify specific biomarkers by screening serum autoantibodies in SAPHO patients with a 17K human whole-proteome microarray. The serum anti-Sp17 autoantibody was identified and verified to be a specific biomarker in patients with SAPHO syndrome. Indeed, the level of the anti-Sp17 autoantibody was significantly increased in patients with active SAPHO compared to patients with an inactive disease and healthy controls (P < 0.05). Additionally, serum anti-Sp17 autoantibody levels correlated with those of serum hypersensitive C-reactive protein (hsCRP), the erythrocyte sedimentation rate (ESR), and ß-crosslaps (ß-CTx) in patients with active SAPHO disease. Moreover, anti-Sp17 autoantibody levels were markedly decreased after anti-inflammatory treatment with pamidronate disodium, which downregulated levels of hsCRP and ESR in patients with active SAPHO. Thus, serum levels of the anti-Sp17 autoantibody might serve as a specific biomarker for the diagnosis of SAPHO syndrome or for monitoring the disease status.

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