ABSTRACT
Objective: Microarray chip was used to detect the differentially expressed microRNA (miRNA) in kidney tissues of rats with kidney-Yang deficiency induced by adenine,and its significance was analyzed by bioinformatics method. Method: Rats with kidney-Yang deficiency were induced by intragastric administration of 150 mg·kg-1 adenine in model group, while rats in normal group were given the same amount of saline.Kidney tissues were taken for hematoxylin-eosin (HE) staining pathological sections after anesthesia and blood urea nitrogen (BUN), creatinine (SCr) in blood and 24-hour urinary protein (24U-TP) in urine were measured. μParaflo microfluidic chip technology was used to investigate differential expression miRNA in kidney tissues, and microarray results were verified by Real-time PCR. Bioinformatics database was used to analyze the target genes and functions of differential expression miRNAs. Result: Gene chip results showed that there were 50 differentially expressed microRNAs after modeling. Compared with control group, only 9 miRNAs were highly expressed in kidney tissues with significant difference were detected in model group. Compared with the normal group, the expression of rno-miR-21-5p, rno-let-7i-5p, rno-miR-146b-5p and rno-miR-15b-5p in model group increased significantly(PPPPPConclusion: This experiment found 4 miRNAs involved in the regulation of renal interstitial fibrosis (RIF) and 2miRNAs with unknown functions, which provided a new clue for further analysis of the regulatory network of kidney-yang deficiency.
ABSTRACT
This study was aimed to investigate the protective effect and mechanism of β-asarone on the animal model of Alzheimer's disease(AD) which was induced by intracerebroventricular injection of Aβ₁₋₄₂ combined cerebral ischemia. One hundred and five rats were randomly divided into seven groups including sham-operated group, AD model group, β-asarone 10 mg•kg⁻¹ group, β-asarone 20 mg•kg⁻¹ group, β-asarone 30 mg•kg⁻¹ group, donepezil group(0.75 mg•kg⁻¹) and Ginkgo biloba extract group(24 mg•kg⁻¹). Rats' learning and memory abilities, cerebric regional blood flow, pathological changes in hippocampal CA1 region, the expression level of HIF-1α and serum CAT, SOD and MDA level were detected 4 weeks later. The results showed that the application of intracerebroventricular injection of Aβ₁₋₄₂ joint 2-VO could lead to rats' dysfunction of learning and memory, decrease in regional cerebral blood flow. Neurons in CA1 region were arranged in disorder, and amyloid deposition was increased. The number of cerebral cortical cells expressing HIF-1α was increased as well. The level of serum CAT and SOD decreased, while level of serum MDA increased. However these symptoms were improved by 20 mg•kg⁻¹ and 30 mg•kg⁻¹ β-asarone. The results indicated that β-asarone could effectively relieve the symptoms of the AD model induced by intracerebroventricular injection of Aβ₁₋₄₂ combined cerebral ischemia, and the potential mechanism might be that it could attenuate damage of MDA to the body by improving the level of CAT and SOD, meanwhile the level of HIF-1α decreased as the decline of hyperoxide which might attenuate its damage to neuron, so it finally achieved alleviating Alzheimer's disease.