RESUMO
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
AIMS: Hyperbaric oxygen preconditioning (HBOP) attenuates brain edema, microglia activation, and inflammation after intracerebral hemorrhage (ICH). In this present study, we investigated the role of HBOP in ICH-induced microglia polarization and the potential involved signal pathway. METHODS: Male Sprague-Dawley rats were divided into three groups: SHAM, ICH, and ICH + HBOP group. Before surgery, rats in SHAM and HBOP groups received HBO for 5 days. Rats in SHAM group received needle injection, while rats in ICH and ICH + HBOP groups received 100 µL autologous blood injection into the right basal ganglia. Rats were euthanized at 24 hours after ICH, and the brains were removed for immunohistochemistry and Western blotting. Neurological deficits and brain water content were determined. RESULTS: Intracerebral hemorrhage induced brain edema, which was significantly lower in the HBOP group. The levels of MMP9 were also less in the HBOP group. HBO pretreatment resulted in less neuronal death and neurological deficits after ICH. Their immunoactivity and protein levels of M1 markers were downregulated, but the M2 markers were unchanged by HBOP. In addition, ICH-induced pro-inflammatory cytokine (TNF-α and IL-1ß) levels and the phosphorylation of JNK and STAT1 were also lower in the HBOP rats. CONCLUSIONS: HBO pretreatment attenuated ICH-induced brain injuries and MMP9 upregulation, which may through the inhibiting of M1 polarization of microglia and inflammatory signal pathways after ICH.
Assuntos
Lesões Encefálicas/metabolismo , Polaridade Celular/fisiologia , Hemorragia Cerebral/metabolismo , Oxigenoterapia Hiperbárica/métodos , Precondicionamento Isquêmico/métodos , Microglia/metabolismo , Animais , Lesões Encefálicas/patologia , Lesões Encefálicas/terapia , Hemorragia Cerebral/patologia , Hemorragia Cerebral/terapia , Mediadores da Inflamação/antagonistas & inibidores , Mediadores da Inflamação/metabolismo , Masculino , Distribuição Aleatória , Ratos , Ratos Sprague-DawleyRESUMO
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.