The Combined Therapy of Berberine Treatment with lncRNA BACE1-AS Depletion Attenuates Aß25-35 Induced Neuronal Injury Through Regulating the Expression of miR-132-3p in Neuronal Cells.

Accumulating articles reported that berberine (Ber) played a neuroprotective role in Alzheimer's disease (AD). Long noncoding RNAs (lncRNAs) have been identified as biomarkers and therapeutic targets of AD. However, the precise mechanism by which lncRNA ß-amyloid cleaving enzyme 1 antisense RNA (BACE1-AS)regulates the progression of AD remains largely unknown. HPN and SK-N-SH cells treated with amyloid ß 25-35 (Aß25-35) were regarded as AD model in vitro. Cell survival rate was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Lactate dehydrogenase (LDH) cytotoxicity assay was conducted to detect the cytotoxicity of neuronal cells. Flow cytometry was performed to determine the intracellular concentration of Ca2+, reactive oxygen species (ROS) and apoptosis of neuronal cells. Western blot assay was carried out to detect the apoptosis-related proteins of neuronal cells. The abundance of lncRNA BACE1-AS and miR-132-3p was measured by quantitative real time polymerase chain reaction (qRT-PCR). The binding sites between miR-132-3p and BACE1-AS were predicted by Starbase, and the combination was confirmed by dual-luciferase reporter assay. We found that Ber alleviated Aß25-35 induced neuronal injury in AD model, especially in high concentration Ber group. The enrichment of BACE1-AS was positively regulated by Aß25-35 and was inversely modulated by Ber in neuronal cells. The interference of BACE1-AS alleviated the neuronal damage of AD model. miR-132-3p was a direct target of lncRNA BACE1-AS in HEK293T cells, and it was negatively regulated by BACE1-AS in neuronal cells. BACE1-AS accumulation reversed the protective effect of miR-132-3p overexpression on AD model. Ber treatment and BACE1-AS intervention recovered the viability of AD model. Ber up-regulated the level of miR-132-3p via BACE1-AS in SK-N-SH and HPN neuronal cells. in conclucsion, Ber protected neuronal cells against Aß25-35 at least partly through BACE1-AS/miR-132-3p axis. The combined therapy of Ber treatment with BACE1-AS depletion might provide new insight into AD treatment.

Upper Limb Ischemic Postconditioning as Adjunct Therapy in Acute Stroke Patients: A Randomized Pilot.

OBJECTIVE: This study aims to observe the clinical effect of upper limb ischemic postconditioning (LIPostC) as an adjunct to treatment with acute stroke patients, possibly due to increased cerebral perfusion. METHODS: We perform a randomized blinded placebo controlled trial in nonthrombolysis patients with acute ischemic stroke, within 72hours of ictus, divided into the LIPostC group and control group. The LIPostC group is induced by 4 cycles of intermittent repeated limb ischemia: alternating 5 minutes inflation (20mm Hg above systolic blood pressure) and 5 minutes deflation performed manually using a standard upper arm blood pressure cuff in the nonparetic arm. The control group receives a sham procedure (cuff inflation to 30mm Hg). Patients underwent the intervention from the time of enrollment to Day 14. Comparison of National Institutes of Health Stroke Scale (NIHSS) score, cerebral infarction volume, relative Perfusion weighted imaging (PWI) parameters (regional relative cerebral blood flow, regional relative mean transit time; preintervention [day 0], day 14, day 90), modified Rankin Scale (mRS; the preintervention score [day 0], the curative ratio at day 90 [we define 0-1 score as close to recovery or full recovery]). RESULTS: Sixty eligible patients with acute stroke (29 LIPostC and 31 control) are recruited age 65years (SD 12.22), blood pressure 156/74mm Hg (SD 14/10), and NIHSS score 5.98 (SD 3.35), mRS score 2.25 (SD .79). Only 1 in the LIPostC group is intolerant the first cycle to give up. All patients tolerate the sham procedure. Two patients experience recurrent stroke versus none in the LIPostC group. Day 90, compared with the control group, there is a significant decrease the NIHSS score, regional relative mean transit time (P < .05) and increase the curative ratio of mRS, regional relative cerebral blood flow(P < .05) in the LIPostC group, which infarct volume decreased by 31.3% (P < .05). CONCLUSIONS: LIPostC after acute stroke is well tolerated and appears safe and feasible. LIPostC may improve neurological outcome, and protective mechanisms may be increased cerebral blood flow to improve cerebral perfusion. A larger trial is warranted.

Oxidation of acetone over Co-based catalysts derived from hierarchical layer hydrotalcite: Influence of Co/Al molar ratios and calcination temperatures.

In order to enhance catalytic performance for acetone, Co-based catalysts prepared under different Co/Al molar ratios and calcination temperatures have been studied in this work. The results indicated that the catalytic activities of the catalysts firstly increased and then decreased with the increase of the Co/Al molar ratio and decreased with the increase of the calcination temperature. Based on the catalytic activities, TG/DTA, XRD, TPR and XPS characterization results, it can be found that catalytic activities of the catalysts with various Co/Al molar ratios were effected by the good crystallization structure of catalyst precursor, surface Co3+/Co2+ molar ratio, low temperature reducibility, and Oads/Olatt molar ratio of the catalysts. Meanwhile, the catalytic activities of the catalysts with different calcination temperatures depended on the low temperature reducibility, surface Co3+/Co2+ molar ratio, porous structure and crystallization structure of the catalyst. Among different synthetic composition, 5:1 CoAlO-300 catalyst (T90% = 225 °C) and 5:1 CoAlO-200 catalyst (T90% = 222 °C) exhibited the efficient acetone oxidation.