[Effects of cinepazide maleate injection on blood pressure in patients with acute ischemic stroke and hypertension].

Objective: To investigate the blood pressure change in patients with acute ischemic stroke (AIS) and hypertension treated with cinepazide maleate injection. Methods: This was a subgroup analysis of post-marketing clinical confirmation study of cinepazide maleate injection for acute ischemic stroke: a randomized, double-blinded, multicenter, placebo-parallel controlled trial, which conducted in China from August 2016 to February 2019. Eligible patients fulfilled the inclusive criteria of acute anterior circulation ischemic stroke with National Institutes of Health Stroke Scale (NIHSS) scores of 7-25. The primary endpoints were mean blood pressure of AIS patients treated with cinepazide maleate or control, which were assessed during the treatment period (14 days), and the proportion of the patients with normal blood pressure was analyzed after the treatment period. Furthermore, a subgroup analysis was performed to investigate a possible effect of the history of hypertension on outcomes. Results: This analysis included 809 patients with hypertension. There was no significant difference in patients blood pressure and the proportion of patients with normal blood pressure (60.5% vs. 59.0%,P>0.05) between cinepazide maleate group and control group. Conclusion: Administration of cinepazide maleate injection does not affect the management of clinical blood pressure in patients with AIS.

MiR-122 regulates cell apoptosis and ROS by targeting DJ-1 in renal ischemic reperfusion injury rat models.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-122 regulates cell apoptosis and ROS by targeting DJ-1 in renal ischemic reperfusion injury rat models, by X.-H. Qu, K. Zhang, published in Eur Rev Med Pharmacol Sci 2018; 22 (24): 8830-8838-DOI: 10.26355/eurrev_201812_16651-PMID: 30575925" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16651.

MiR-122 regulates cell apoptosis and ROS by targeting DJ-1 in renal ischemic reperfusion injury rat models.

OBJECTIVE: Phosphatidylinositol 3-kinase/protein kinase B ((PI3K/AKT) signaling pathway plays a role in regulating cell survival and apoptosis. Phosphatase and tensin homologue deleted on chromosome ten (PTEN) can negatively regulate PI3K/AKT signaling pathway, while DJ-1 (Parkinson gene 7) can negatively regulate expression and function of PTEN. DJ-1-PTEN/PI3K/AKT signaling pathway plays a role in the regulation of ischemic reperfusion (IR) injury. Bioinformatics analysis showed that there was a targeted complementary binding site between microRNA-122 (miR-122) and 3'-UTR of DJ-1 mRNA. This study aimed to investigate the effects of miR-122 in regulating DJ-1-PTEN/PI3K/AKT signaling pathway and acute renal I-R injury. MATERIALS AND METHODS: Rat renal artery was clamped and restored after 30 min to establish renal IR injury model. Renal tissue samples were collected at 10 h and 20 h after operation. miR-122 and DJ-1 mRNA were detected with quantitative Real-time PCR (qRT-PCR). DJ-1 protein was tested by using Western blot. Blood urea nitrogen (BUN) and serum creatinine (SCr) were measured. Rat tubular epithelial cells, RRTEC, were cultured in vitro and divided into transfection (miR-NC group) and treatment group (miR-122 inhibitor group). IR treatment was performed after 72 h of transfection. DJ-1, PTEN, AKT, and phosphorylated AKT (p-AKT) were detected using Western blot. Cell apoptosis and reactive oxygen species (ROS) were measured with flow cytometry. RESULTS: Compared with Sham group, blood BUN and SCr contents significantly increased (p < 0.05), miR-122 level significantly elevated (p < 0.05), while DJ-1 mRNA and protein markedly declined (p < 0.05) in IR model rats. Compared with control group, I-R treatment significantly up-regulated miR-122 and PTEN expressions (p < 0.05), decreased DJ-1 and p-AKT levels (p < 0.05), and induced apoptosis and ROS production (p < 0.05) in RRTEC cells. Transfection with miR-122 inhibitor markedly up-regulated DJ-1 expression (p < 0.05), enhanced PTEN/PI3K/AKT pathway activity (p < 0.05), and reduced apoptosis and ROS production (p < 0.05). CONCLUSIONS: MiR-122 increased significantly, while DJ-1 declined significantly during renal I-R injury. Down-regulation of miR-122 markedly elevated DJ-1, enhanced PTEN/PI3K/AKT pathway activity, and inhibited apoptosis and ROS generation in rat renal tubular epithelial cells to alleviate IR injury.

Mechanical properties, in vitro corrosion resistance and biocompatibility of metal injection molded Ti-12Mo alloy for dental applications.

A biocompatible Ti-12Mo alloy was fabricated by metal injection moulding (MIM) using non-spherical titanium, molybdenum powders and a purposely designed binder. The density, microstructure and tensile properties were characterized. This was followed by a detailed assessment of its in vitro corrosion and biocompatibility performances, compared with that of two commonly used titanium-based materials extra low interstitial (ELI) Ti-6Al-4V and commercially pure (CP) titanium. The MIM-fabricated Ti-12Mo alloy can achieve a wide range of mechanical properties through controlling sintering process. Specimens sintered at 1400 °C are characterized by fairly uniform near-ß microstructure and high relative density of 97.6%, leading to the highest tensile strength of 845.3 ±â€¯21 MPa and elongation of 4.15 ±â€¯0.2% while the highest elastic modulus of 73.2 ±â€¯5.1 GPa. Owing to the formation of protective TiO2-MoO3 passive film, the MIM-fabricated Ti-12Mo alloy exhibits the highest corrosion resistance including the noblest corrosion potential, the lowest corrosion current density and the highest pitting potential in four different electrolytes. The in vitro cytotoxicity test suggests that the MIM-fabricated Ti-12Mo alloy displays no adverse effect on MC3T3-E1 cells with cytotoxicity ranking of 0 grade, which is nearly close to ELI Ti-6Al-4V or CP Ti. These properties together with its easy net-shape manufacturability make Ti-12Mo an attractive new dental implant alloy.

Andrographolide suppresses RANKL-induced osteoclastogenesis in vitro and prevents inflammatory bone loss in vivo.

BACKGROUND AND PURPOSE: Osteoclasts play a pivotal role in diseases such as osteoporosis, rheumatoid arthritis and tumour bone metastasis. Thus, searching for natural compounds that may suppress osteoclast formation and/or function is promising for the treatment of osteoclast-related diseases. Here, we examined changes in osteoclastogenesis and LPS-induced osteolysis in response to andrographolide (AP), a diterpenoid lactone isolated from the traditional Chinese and Indian medicinal plant Andrographis paniculata. EXPERIMENTAL APPROACH: Effects of AP on osteoclast differentiation and bone resorption were measured in vitro. Western blots and RT-PCR techniques were used to examine the underlying molecular mechanisms. The bone protective activity of AP in vivo was assessed in a mouse model of osteolysis. KEY RESULTS: AP concentration-dependently suppressed RANKL-mediated osteoclast differentiation and bone resorption in vitro and reduced the expression of osteoclast-specific markers, including tartrate-resistant acid phosphatase, calcitonin receptors and cathepsin K. Further molecular analysis revealed that AP impaired RANKL-induced NF-κB signalling by inhibiting the phosphorylation of TGF-ß-activated kinase 1, suppressing the phosphorylation and degradation of IκBα, and subsequently preventing the nuclear translocation of the NF-κB p65 subunit. AP also inhibited the ERK/MAPK signalling pathway without affecting p38 or JNK signalling. CONCLUSIONS AND IMPLICATIONS: AP suppressed RANKL-induced osteoclastogenesis through attenuating NF-κB and ERK/MAPK signalling pathways in vitro, thus preventing bone loss in vivo. These data indicated that AP is a promising natural compound for the treatment of osteoclast-related bone diseases.

An external-sample liquid scintillation counting for 75Se and its application to selenoprotein detection.

An external-sample liquid scintillation (LS) counting for the gamma emitter 75Se has been developed. An expressly designed well-type LS vial and a 2,5-diphenyoxazole-1,4-bis(5-phenyl-2-oxazoyl)-benzene-xylene solution containing 35% tertrabutylzinn allow 75Se to be counted in a standard LS counter with counting efficiency up to 43.2%, much higher than that of conventional LS counting method. This external sample LS has a good count rate linearity and exhibits low background count rates. After in vivo labeling with [75Se]selenite, 75Se distributions and the Se-containing proteins present in tissues of male rat were investigated by means of sodium dodecyl sulfate-polyacrylamide gel electrophoresis, external-sample LS and gamma-detector. Eight Se-containing proteins or protein subunits were detected to be Se-containing proteins or protein subunits in arterial wall, and their apparent molecular masses (Mr) were 76.4, 67.0, 57.4, 30.3, 25.4, 22.7, 21.7, and 15.1 kDa, respectively. In addition, eight 75Se-labeled proteins (Mr: 66.8, 57.0, 43.1, 30.0, 24.8, 19.8, 18.0, and 14.8 kDa) were found in brain homogenates, and nine 75Se-labeled proteins (Mr: 117.0, 78.0, 66.6, 57.2, 43.0, 38.1, 25.0, 20.1, and 18.0 kDa) were detected in testis homogenates. Some of them should be new biologically important selenoproteins that have not been identified so far.