Hyperuricemic Nephropathy in Traditional Chinese Medicine and Integrated Traditional Chinese and Western Medicine： A Review / 中国实验方剂学杂志

Hyperuricemic nephropathy （HN）， a secondary renal damage common in clinical practice， is characterized by early concealing and continuous progression. The understanding of HN in traditional Chinese medicine （TCM） is from a macroscopic perspective. According to the TCM theory， HN is caused by the combination of external pathogens and internal injuries， with the main pathogenesis being root deficiency combined with superficial excess and deficiency-excess in complexity. In western medicine， the understanding of HN is from the microscopic perspective， which holds that the occurrence of HN is the result of inflammation， oxidative stress， renin-angiotensin-aldosterone system （RAAS） activation， and metabolic abnormalities. The TCM syndromes of HN include internal dampness and heat， obstruction in dampness and turbidity， deficiency of spleen and kidney， and deficiency of kidney yin. Accordingly， the prescriptions should clear heat and dampness， remove dampness and turbidity， tonify spleen and kidney， and nourish kidney yin， respectively. In addition to TCM prescriptions， single herbal medicines and their extracts， Chinese patent medicines， and external applications of Chinese medicines have played a significant role in the treatment of HN， promoting the application of TCM in the treatment of HN. Moreover， the integrated traditional Chinese and western medicine has also played a role in the treatment of HN， enriching the treatment schemes of HN. Different from common kidney diseases such as acute and chronic glomerulonephritis and nephrotic syndrome， HN with particularity should be carefully differentiated in clinical practice. This article systematically summarizes the research progress in the treatment of traditional Chinese medicine and integrated traditional Chinese and western medicine on hyperuricemic nephropathy with TCM and integrated traditional Chinese and western medicine， aiming to enrich the system and theory of HN treatment and further guide the clinical practice.

Research progress on the roles of neurovascular unit in stroke-induced immunosuppression / 浙江大学学报·医学版

A complex pathophysiological mechanism is involved in the brain injury following cerebral infarction. The neurovascular unit (NVU) is a complex multi-cellular structure consisting of endothelial cells , neurons, glia, smooth muscle cells, and pericytes. The dyshomeostasis of NVU directly participates in the inflammatory immune regulation process. The components of NVU promote inflammatory overreaction and also synergize with the overactivation of autonomic nervous system to initiate stroke-induced immunosuppression (SIID). SIID can alleviate the damage caused by inflammation, however, it also makes stroke patients more susceptible to infection, leading to systemic damage and worsening the condition. This article reviews the mechanism of SIID and the roles of NVU components in SIID, to provide a perspective for recanalization, prognosis and immune regulation therapy of cerebral infarction.

Construction of point mutation rabbits using CRISPR/Cas9 / 浙江大学学报·医学版

To establish a rabbit model of proprotein convertase subtilisin/kexin type9 () point mutation with CRISPR/Cas9 gene editing technique. According to the PubMed gene protein data, the PCSK9 protein functional regions of human and rabbit were analyzed by Blast. The 386S (Ser) amino acid functional region of human gene was homologous to the 485S of rabbit gene. Three small guide RNAs and one single-stranded donor oligonucleotide were designed according to the 485S base substitution position and sequence analysis of rabbit gene. The synthetic small guide RNAs, Cas9 mRNA and single-stranded donor oligonucleotide were co-injected into the cytoplasm of rabbit fertilized eggs and the embryos were transferred into the pregnant rabbits. PCR, TA cloning and off-target analysis were performed on the F0 rabbits to identify whether the PCSK9 mutation was successful. Fifteen F0 rabbits were obtained. The sequencing results showed that one of them was PCSK9 point mutation homozygote and two of them were PCSK9 point mutation heterozygotes, and the mutation could be stably inherited. The rabbit model of PCSK9 point mutation was successfully constructed by CRISPR/Cas9 technique, which provides an animal model for exploring the molecular mechanism of impaired PCSK9 function and developing reliable and effective diagnosis and treatment measures.

Research advance of Nrf2 on atherosclerosis by regulating vascular smooth muscle cell / 浙江大学学报·医学版

Atherosclerosis is a common pathological change in cardiovascular disease. Vascular smooth muscle cell is the main source of plaque cell and extracellular matrix, and nuclear factor-erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating the function of vascular smooth muscle cell. In the process of atherosclerosis, Nrf2 signaling pathway has the following regulatory effects on vascular smooth muscle cell: regulating the phenotype of vascular smooth muscle cell to change to the direction conducive to the alleviation of disease progression; inhibiting the proliferation and migration of vascular smooth muscle cell; mitigating the level of blood lipid; alleviating vascular smooth muscle cell calcification, aging and apoptosis process. This article reviews the specific mechanisms of Nrf2 regulating atherosclerosis, such as phenotypic transformation, proliferation and migration, lipid metabolism, calcification, aging and apoptosis in atherosclerosis, in order to provide a basis for understanding the molecular mechanism of atherosclerosis development and finding therapeutic targets.

Correlation between serum miR-320b and carotid atherosclerosis in patients with acute ischemic stroke / 国际脑血管病杂志

Objective To investigate the correlation between serum miR-320b and carotid atherosclerosis in patients with acute ischemic stroke.Methods From January 2017 to December 2017,patients with acute ischemic stroke visited the Department of Neurology,the Affiliated Hospital of Yangzhou University were enrolled.According to the findings of carotid artery ultrasonography,they were divided into plaque group and plaque-free group.The baseline clinical data such as demographic data,vascular risk factors,and blood biochemical indicators were collected.Reverse transcription quantitative polymerase chain reaction was used to detect the expression level of serum miR-320b.Multivariatelogistic regression analysis was used to determine the independent risk factors for carotid atherosclerosis.Results A total of 135 patients with acute ischemic stroke were enrolled in this study,including 58 females and 77 males,aged 58.4 ± 10.6 years.There were 85 patients in the plaque group and 50 in the plaque-free group.The total cholesterol (t =5.523,P =0.023) and low-density lipoprotein cholesterol (t =4.415,P =0.044) in the plaque group were significantly higher than those in the plaque-free group,while high-density lipoprotein cholesterol (t =5.849,P=0.017) and serum miR-320b (t =4.331,P=0.039) were significantly lower than those in the plaque-free group.Multivariate logistic regression analysis showed that referring to the highest quartile group,the low serum miR-320b level might be an independent risk factor for carotid atherosclerosis (the first quartile group:odds ratio 2.701,95％ confidence interval 1.154-6.321,P =0.022;the second quartile group:odds ratio 2.521,95％ confidence interval 1.249-5.091,P =0.010;and the third quartile group:odds ratio 1.849,95％ confidence interval 1.041-3.283,P=0.036).Conclusion The low serum miR-320b level might be an independent risk factor for carotid atherosclerosis in patients with acute ischemic stroke.

Dynamic changes of ATP binding cassette transporter A1 expression in perihematomal tissue of mouse cerebral hemorrhage model induced by collagenase / 国际脑血管病杂志

Objective To investigate the ATP binding cassette transporter A1 (ABCA1) expression in perihematomal tissue of mouse cerebral hemorrhage model induced by collagenase. Methods Stereotactic injection of type Ⅳ collagenase was used to induce a model of caudate putamen intracerebral hemorrhage in mice. The behavioral scores were use to assess neurological deficits at 24 h, 48 h and 72 h after model making. Neisserian staining was used to detect the morphology of neurons around hematomas.Immunohistochemical staining and Western blot analysis were used to detect the expression of ABCA1 around hematomas. Results Nissl bodies reduction, atrophy, necrosis of perihematomal neurons were observed and aggravated over time. Immunohistochemical staining and Western blot analysis showed that the expression level of ABCA1 in the perihematomal tissue was significantly higher than that in the sham operation group (all P < 0. 05), and the expression level increased significantly with time (all P < 0. 05 ).Conclusion ABCA1 was up-regulated after cerebral hemorrhage, suggesting that it might be involved in the pathological process of cerebral hemorrhage.

Cerebral white matter injury and repair after intracerebral hemorrhage / 国际脑血管病杂志

Animal experiments and clinical studies have shown that intracerebral hemorrhage may damage the white matter.The pathophysiology mechanisms of cerebral white matter injury and repair after intracerebral hemorrhage is very complicated.This article reviews the related clinical and experimental evidence,pathophysiological mechanisms,and possible intervention strategies of cerebral white matter injury after intracerebral hemorrhage.