RESUMO
Clinical and experimental data have demonstrated that inflammation plays fundamental roles in the pathogenesis of ischemic stroke. Interleukin-16 (IL-16) is identified as a proinflammatory cytokine that is a key element in the ischemic cascade after cerebral ischemia. We aimed to examine the relationship between the IL-16 polymorphisms and the risk of ischemic stroke in a Chinese population. A total of 198 patients with ischemic stroke and 236 controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing method. We found that the rs11556218TG genotype and G allele of IL-16 were associated with significantly increased risks of ischemic stroke (TG versus TT, adjusted OR = 1.88; 95% CI, 1.15-3.07; G versus T, adjusted OR = 1.54; 95% CI, 1.05-2.27, resp.). However, there were no significant differences in the genotype and allele frequencies of IL-16 rs4778889 T/C and rs4072111 C/T polymorphisms between the two groups, even after stratification analyses by age, gender, and the presence or absence of hypertension, diabetes mellitus, hypercholesterolemia, and hypertriglyceridemia. These findings indicate that the IL-16 polymorphism may be related to the etiology of ischemic stroke in the Chinese population.
Assuntos
Isquemia Encefálica/patologia , Interleucina-16/genética , Polimorfismo Genético , Acidente Vascular Cerebral/patologia , Idoso , Alelos , Povo Asiático , Estudos de Casos e Controles , China , Feminino , Frequência do Gene , Genótipo , Humanos , Leucócitos/citologia , Masculino , Pessoa de Meia-Idade , Razão de Chances , Polimorfismo de Fragmento de Restrição , Fatores de Risco , Análise de Sequência de DNARESUMO
BACKGROUND: Paraneoplastic cerebellar degeneration (PCD), which is rare in clinical practice, is closely related to autoimmunity. Cases positive for anti-Yo antibodies (anti-Purkinje cytoplasmic antibody 1) are the main subtype of PCD. PCD is subacute cerebellar degeneration, and while it progresses over weeks to months, its resultant deficits last much longer. Cancer patients with anti-Yo antibody-positive PCD are very rare. Most of them are breast cancer or ovarian cancer patients but also occasionally lung cancer patients. CASE SUMMARY: A 61-year-old woman presented with sudden vertigo, nausea, and vomiting for approximately 10 d. The patient's neurological examination showed torsion with downbeat nystagmus and ataxia of the right limb and trunk. Laboratory examination found that the patient's cerebrospinal fluid and serum were anti-Yo antibody-positive, positron emission tomography computed tomography showed an increased metabolic rate in the retroperitoneal lymph nodes, and the pathology of lymph node punctures in the retroperitoneum and neck suggested adenocarcinoma of the pancreaticobiliary duct, which strengthens the hypothesis of paraneoplastic origin. Intravenous immunoglobulin (IVIg) 0.4 g/kg/d for 5 d and methylprednisolone 160 mg for 3 d were initiated, which was reduced to 80 mg for 3 d and then to 40 mg for 7 d. After treatment with IVIg and a steroid, the patient's vertigo and ataxia alleviated. CONCLUSION: The patient's vertigo and ataxia alleviated after treatment, suggesting that early immunotherapeutic intervention may have certain value in stopping neurological loss.
RESUMO
Background: Rhodiola rosea L. has long been used as traditional medicines in Europe and Asia to treat a variety of common conditions and diseases including Alzheimer's disease, cardiovascular disease, cognitive dysfunctions, cancer, and stroke. Previous studies reported that Rhodiola rosea L. and its components (RRC) improve ischemia stroke in animal models. Here, we conducted a systematic review and meta-analysis for preclinical studies to evaluate the effects of RRC and the probable neuroprotective mechanisms in ischemic stroke. Methods: Studies of RRC on ischemic stroke animal models were searched in seven databases from inception to Oct 2021. The primary measured outcomes included the neural functional deficit score (NFS), infarct volume (IV), brain water content, cell viability, apoptotic cells, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells, B-cell lymphoma-2 (Bcl-2) level and tumor necrosis factor-α (TNF-α) level. The secondary outcome measures were possible mechanisms of RRC for ischemic stroke. All the data were analyzed via RevMan version 5.3. Results: 15 studies involving 345 animals were identified. Methodological quality for each included studies was accessed according to the CAMARADES 10-item checklist. The quality score of studies range from 1 to 7, and the median was 5.53. Pooled preclinical data showed that compared with the controls, RRC could improve NFS (Zea Longa (p < 0.01), modified neurological severity score (mNSS) (p < 0.01), rotarod tests (p < 0.01), IV (p < 0.01), as well as brain edema (p < 0.01). It also can increase cell viability (p < 0.01), Bcl-2 level (p < 0.01) and reduce TNF-α level (p < 0.01), TUNEL-positive cells (p < 0.01), apoptotic cells (p < 0.01). Conclusion: The findings suggested that RRC can improve ischemia stroke. The possible mechanisms of RRC are largely through antioxidant, anti-apoptosis activities, anti-inflammatory, repressing lipid peroxidation, antigliosis, and alleviating the pathological blood brain barrier damage.
RESUMO
The present study aimed to examine how the long noncoding RNA (lncRNA) RP11543N12.1 interacted with microRNA (miR)3243p to modify microglials (MIs)induced neuroblastoma cell apoptosis, which may pose benefits to the treatment of Alzhemier's disease (AD). The cell model of AD was established by treating SHSY5Y cells with amyloid ß (Aß)2535, and MI were acquired using primary cell culture technology. The lncRNAs that were differentially expressed between SHSY5Y and control cells were screened through a microarray assay and confirmed via polymerase chain reaction. In addition, overexpression of RP11543N12.1 and miR3243p was established by transfection of SHSY5Y cells with pcDNA3.1(+)RP11543N12.1 and miR3243p mimics, respectively, while downregulation of RP11543N12.1 and miR3243p was achieved by transfection with RP11543N12.1small interfering RNA (siRNA) and miR3243p inhibitor, respectively. The interaction between RP11543N12.1 and miR3243p was confirmed with a dualluciferase reporter gene assay. The results revealed that the expression levels of total and phosphorylated tau in SHSY5Y cells were significantly elevated following Aß2535 treatment (P<0.05), and RP11543N12.1 was found to be differentially expressed between the control and Aß2535treated cells (P<0.05). Furthermore, the targeted association of RP11543N12.1 and miR3243p was predicted based on miRDB4.0 and PITA databases, and then validated via the dualluciferase reporter gene assay. SHSY5Y cells transfected with siRNA or inhibitor, and treated with Aß2535 displayed cellular survival and apoptosis that were similar to the normal levels (P<0.05). Finally, coculture of MI and SHSY5Y cells transfected with RP11543N12.1siRNA/miR3243p inhibitor significantly enhanced cell apoptosis (P<0.05). In conclusion, RP11543N12.1 targeted miR3243p to suppress proliferation and promote apoptosis in the AD cell model, suggesting that RP11543N12.1 and miR3243p may be potential biomarkers and therapeutic targets for AD.
Assuntos
Apoptose/genética , Regulação da Expressão Gênica , Inflamação/genética , Inflamação/patologia , MicroRNAs/metabolismo , Microglia/patologia , Neurônios/patologia , RNA Longo não Codificante/metabolismo , Doença de Alzheimer/genética , Doença de Alzheimer/patologia , Sequência de Bases , Linhagem Celular Tumoral , Sobrevivência Celular/genética , Feminino , Perfilação da Expressão Gênica , Humanos , MicroRNAs/genética , Microglia/metabolismo , Modelos Biológicos , Neurônios/metabolismo , RNA Longo não Codificante/genética , Proteínas tau/metabolismoRESUMO
OBJECTIVE: Interleukin-6 (IL-6) is a pleiotropic cytokine and important mediator of many inflammatory processes, which might affect susceptibility to multiple sclerosis (MS). The aim of this study was to assess the effect of IL-6-174G/C polymorphism on the risk of MS using a meta-analysis. MATERIALS AND METHODS: The Pubmed, ISI Web of Science, Wanfang, VIP, and China National Knowledge Infrastructure databases were screened and six studies were included in the meta-analysis. Pooled odds ratios (ORs) with corresponding 95% confidence intervals (CI) were calculated to evaluate the association between the IL-6-174G/C polymorphism and risk of MS. RESULTS: No significant association between the IL-6-174G/C polymorphism and risk of MS was observed in overall analyses. With stratification according to ethnicity, we found that carriers with the IL-6-174CC genotype had a 1.87-fold increased risk for the development of MS in Asians (recessive model: OR=1.87, 95% CI, 1.08-3.24), but not in Caucasians. CONCLUSION: This meta-analysis provides evidence that the IL-6-174G/C polymorphism may be a risk factor for the development of MS in Asians. Further association studies with a larger sample size are required to confirm the result in different populations.