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Crystal structures and magnetic properties are determined for two novel compounds, [1-(4'-iodobenzyl)-pyridinium][M(mnt)(sub 2)] (mnt(super 2-) = maleonitriledithiolate, M = Ni (1) or Cu (2)). It is concluded that the structural transition of M=Ni is driven by spin-lattice interaction, as crystal Cu (S = 0) does not exhibit a structural transition.

OBJECTIVE: To investigate the regulatory effects of simvastatin on the inflammation and oxidative stress in rats with cerebral hemorrhage through the nuclear factor E2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway. MATERIALS AND METHODS: A total of 120 healthy male rats weighing 280-300 g and 7-8 weeks old were selected to establish the traumatic brain injury (TBI) model. Rats were divided into group A (trauma operation, n=30), group B (no treatment, n=30), group C (drug administration after trauma operation, n=30), and group D (no trauma operation, drug administration, n=30). Cerebral edema content in brain tissues was measured by calculating the dry and wet weight. Neurological dysfunction was scored using the Garcia method. Positive levels of the Toll-like receptor 4 (TLR4) and interleukin-1β (IL-1β) were qualitatively analyzed via immunohistochemistry. Protein levels of TLR4 and IL-1β were quantitatively analyzed via Western blotting. Moreover, the brain injury volume and neuronal apoptosis were evaluated via Nissl staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. At 48 h after injury, activities of superoxide dismutase (SOD), reduced glutathione (GSH), and oxidized glutathione (GSSG) in brain tissues were detected, and levels of malondialdehyde (MDA) and nitric oxide (NO) were detected using the enzyme activity assay kits. Finally, relative levels of the Nrf2-ARE signaling pathway and its downstream molecules heme oxygenase-1 (HO-1) and NAD (P) H dehydrogenase, quinone 1 (NQO1) were detected via reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting. RESULTS: Compared with those in group B, cerebral edema content in brain tissues significantly increased (p<0.05), the neurological dysfunction score significantly declined (p<0.05), and protein levels of TLR4 and IL-1β were significantly upregulated in group A (p<0.05). In group C, relative levels of TLR4 and IL-1β were down-regulated, cerebral edema content decreased, and the neurological dysfunction score significantly increased (p<0.05). After 48 h, activities of SOD, reduced GSH and GSSG and levels of MDA and NO all increased, and levels of MDA and NO declined in group C (p<0.05). Western blotting and RT-PCR showed that simvastatin could increase the transcriptional level of Nrf2. After simvastatin intervention, expression levels of downstream molecules HO-1 and NQO1 were upregulated. CONCLUSIONS: Simvastatin alleviates TLR4-mediated inflammatory injury, promotes neurological recovery and resists oxidative stress through the Nrf2-ARE signaling pathway, thus exerting a neuroprotective effect in TBI. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the effect of micro-ribonucleic acid (miR)-130a on neuronal injury in rats with intracerebral hemorrhage (ICH) through the phosphatase and tensin homolog deleted on chromosome ten/phosphatidylinositol 3-hydroxy kinase/protein kinase B (PTEN/PI3K/AKT) signaling pathway. MATERIALS AND METHODS: A total of 30 healthy male rats were randomly divided into three groups, including the blank control group, ICH model group (ICH group) and ICH model + miR-130a treatment group (miR-130a treatment group). The differences in neurological injury, the number of apoptotic cells in brain tissues, the activity of Caspase-9 and protein expressions of PTEN/PI3K/AKT were analyzed among the three groups, respectively. RESULTS: Neurological function was normal without injury in the control group. However, the neurological injury was severe in the ICH group and mild in the miR-130a treatment group. There were statistically significant differences in neurological function in the control group relative to those of the ICH group and miR-130a treatment group (p<0.05). Meanwhile, the neurological injury was markedly milder in the miR-130a treatment group than that of the ICH group, showing a statistically significant difference (p<0.05). The number of apoptotic cells was remarkably smaller in the control group when compared with the ICH group and miR-130a treatment group. However, it was markedly larger in the ICH group than that of the miR-130a treatment group, showing significant differences (p<0.05). The activity of Caspase-9 was significantly lower in the control group than ICH group and miR-130a treatment group (p<0.05). However, it increased remarkably in the ICH group compared with that of the miR-130a treatment group (p<0.05). Moreover, the protein level of PTEN in the ICH group was significantly higher than control group and miR-130a treatment group, displaying statistically significant differences (p<0.05). However, no marked difference in the protein level of PTEN was observed between the control group and miR-130a treatment group (p>0.05). The protein levels of the phosphorylated 3-hydroxy kinase (p-PI3K) and phosphorylated protein kinase B (p-AKT) were remarkably lower in the ICH group than those of the control group and miR-130a treatment group, displaying statistically significant differences (p<0.05). However, they were remarkably higher in the miR-130a treatment group than that of the control group (p<0.05). CONCLUSIONS: MiR-130a promotes neuronal growth in brain tissues in ICH rats and alleviates neuronal injury after ICH through the PTEN/PI3K/AKT signaling pathway. Our findings suggest that miR-130a exerts important clinical significance in the treatment of ICH. [ABSTRACT FROM AUTHOR]