ABSTRACT
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-1β 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-1β 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-1β 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-1β 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-1β proteins in rats with cerebral hemorrhage, and protect neurons and reduce secondary inflammatory damages by down-regulating the above protein-mediated inflammatory responses.
ABSTRACT
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-1β 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-1β 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-1β 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-1β 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-1β proteins in rats with cerebral hemorrhage, and protect neurons and reduce secondary inflammatory damages by down-regulating the above protein-mediated inflammatory responses.
ABSTRACT
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).
Subject(s)
Humans , Arthrodermataceae , Cell Biology , Genetics , Hyphae , Cell Biology , RNA, Fungal , Genetics , RNA, Ribosomal, 18S , Genetics , Skin , MicrobiologyABSTRACT
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).
ABSTRACT
Objective To study the effect of progesterone on tumor necrosis factor (TNF-α),interleukin-1β (IL-1β),nerve growth factor(NGF) and brain derived neurotrophic factor(BDNF) expression in the cortex and hippocampus tissue in newborn rats with hypoxic-ischemic brain damage (HIBD),and to discuss the protective molecular mechanism of progesterone on HIBD in neonatal rats.Methods Forty-eight 7-day-old neonatal rats were randomly divided into 3 groups:sham-operated group,hypoxic-ischemic group and pretreatment group.Rats in hypoxic-ischemic group and pretreatment group were subjected to left common carotid artery ligation,then they were exposed to 80 mL/L oxygen and 920 mL/L nitrogen gas in the closed container at 37 ℃ for up to 2.5 h to establish HIBD models.Progesterone was injected intraperitoneally into the rats in the pretreatment group 30 min before hypoxia,and solution was injected into the first 2 groups.All the rats were killed at the 24 h after operation.The levels of TNF-α,IL-1β,NGF,BDNF were measured by enzyme linked immunosorbent assay and the expressions of TNF-α,IL-13,NGF,BDNF mRNA were analyzed by reverse transcription-polymerase chain reaction.Results The contents of TNF-α,IL-1β,NGF,BDNF and their mRNA expressions in hypoxic-ischemic group were significantly higher than those in the sham-operated group.In pretreatment groups,the levels of TNF-α,IL-1β and their mRNA expressions were significantly lower than those in hypoxic-ischemic group.The levels of NGF,BDNF and their mRNA expressions in pretreatment group were significantly higher than those in hypoxic-ischemic group (all P ＜ 0.05).Conclusions Progesterone exerts neuroprotective effect on hypoxic-ischemic encephalopathy-induced brain damage,and the action mechanism is related to down-regulate the expression of damage factor and up-regulate the expression of anti damage factor.