Preventive and therapeutic effect of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage.

OBJECTIVE: To investigate the preventive and therapeutic effect and mechanism of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage. METHODS: Sixty SD rat aged 9-12 weeks were chosen and divided into the control group, model group and simvastatin-treated group randomly with 20 rats in each group. Rats in the model group and simvastatin-treated group were infused with autologous fresh uncoagulated blood to the right brain tissue of the basal ganglia to build the cerebral hemorrhage model, while rats in the control group were treated with the same amount of normal saline. Then, rats in the simvastatin-treated group were given a gavage of 3 mg/kg of simvastatin once a day after modeling. Rats in the three groups were given nerve dysfunction score (NDS) and wet-dry weighting method was used to detect the brain water content (BWC) of brain tissues around the lesion of the rats. Then Nissl staining was conducted and the undamaged neurons were counted. Immunohistochemical SP method was applied to count the number of NF-κB, TLR4 and IL-1ß positive cells in brain tissues around the lesions, and the immuno fluorescence method was employed to determine the expression levels of NF-κB, TLR4 and IL-1ß proteins. RESULTS: The NDS results of the simvastatin-treated group at all time points were all significantly higher than those of the model group (P < 0.05); the BWC values of the simvastatin-treated group at all time points were all significantly lower than those of the model group at the same periods (P < 0.05); the number of the undamaged neurons around the lesions of the simvastatin-treated group at all time points were all significantly higher than those of the model group (P < 0.05); seven days after treatment, the number of the NF-κB, TLR4 and IL-1ß positive cells in brain tissues around the lesions of the simvastatin-treated group were all significantly lower than those of the model group (P < 0.05), and its expression levels of NF-κB, TLR4 and IL-1ß protein were also significantly lower than those of the model group (P < 0.05). CONCLUSIONS: Simvastatin can inhibit the expressions of NF-κB, TLR4 and IL-1ß proteins in rats with cerebral hemorrhage, and protect neurons and reduce secondary inflammatory damages by down-regulating the above protein-mediated inflammatory responses.

Tanshinone IIA prevents the loss of nigrostriatal dopaminergic neurons by inhibiting NADPH oxidase and iNOS in the MPTP model of Parkinson's disease.

Tanshinone IIA is one of the major constituents of Salvia miltiorrhiza Bunge known as Danshen. Recent reports have shown that Tanshinone IIA has neuroprotective effects against cerebral ischemia/reperfusion injury and traumatic injury of the spinal cord in rats. However, whether Tanshinone IIA has any neuroprotective effect in Parkinson's disease remains unknown. In this study, we evaluated whether Tanshinone IIA promotes the survival of nigrostriatal dopaminergic (DA) neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. MPTP induced degeneration of nigrostriatal DA neurons and microglial activation as visualized by tyrosine hydroxylase and CD11b immunoreactivity. The results of Western blot and immunohistochemistry showed upregulation of NADPH oxidase and iNOS in the MPTP-treated substantia nigra pars compacta. Treatment with Tanshinone IIA prevented degeneration of nigrostriatal DA neurons and increased the level of striatal dopamine content. This neuroprotection afforded by Tanshinone IIA was associated with the suppression of microglial activation and reduced expression of NADPH oxidase and iNOS. The present findings show that Tanshinone IIA may possess anti-inflammatory and anti-oxidative properties and may have therapeutic value in the treatment of Parkinson's disease.

Morphological and molecular identification of two strains of dermatophytes.

In this study, we used traditional morphological and molecular identification methods to preliminarily identify two strains of dermatophytes. The two strains were observed under the microscope. And then the dermatophytes were cultured on Sabouraud's dextrose agar (SDA). The 18S rRNA regions of the two dermatophyte strains were amplified by polymerase chain reaction (PCR), and the PCR products were sequenced and compared with GenBank data. BLAST tools and DNAMAN software were used to analyze the sequences. To further determine highly homologous sequences, a phylogenetic tree was constructed using the Neighbor-Joining method. The two strains of dermatophytes were identified by traditional morphological identification as Epidermophyton floccosum and Microsporum ferrugineum. The 18S rRNA sequence analyses showed high similarities to Cladosporium cladosporioides isolate C115LM-UFPR and Ascomycete sp. LB68A1A2. Epidermophyton and Cladosporium belong to dermatophyte, while Microsporum ferrugineum and Ascomycete belong to microsporum. The two novel strains of dermatophytes were therefore identified as Cladosporium cladosporioides isolate C115LM-UFPR (JN650537, Cladosporium) and Ascomycete sp. LB68A1A2 (AY770409, Ascomycete sp).