Effect and mechanism of astragaloside Ⅳ on Toll-like receptor pathway in fibrotic mice after renal ischemia-reperfusion / 中国中药杂志

The aim of this paper is to study the effect of astragaloside Ⅳ on renal fibrosis mice with ischemia-reperfusion injury (IRI) and discuss the mechanism. Male C57BL/6 50 mice were randomly divided into four groups, namely Sham-operated group, model group, AS-Ⅳ prevention group and AS-Ⅳ treatment group. Since the day of surgery, the mice in astragaloside Ⅳ prevention group were treated with astragaloside Ⅳ by gavage for 30 days at the dose of 30 mg·kg⁻¹·d⁻¹. At the 60th day after surgery, the mice in astragaloside Ⅳ treatment group were treated with astragaloside Ⅳ 100 by gavage for 30 days at the dose of 30 mg·kg⁻¹·d⁻¹. The mice in Sham-operated group and model group were treated with double distilled water containing 0.1% ethanol instead of astragaloside Ⅳ. Serum creatinine and blood urea nitrogen were detected by chemical methods. Histopathological changes and collagen deposition of affected kidneys were observed under optical microscope by HE and Masson staining. The expression levels of Toll like receptor pathway related molecules (TLR4,MyD88,TRAF6,TRAM,TRIF,NF-κB,TNF-α,IL-6, IFN-) in affected kidneys were observed by immunohistochemistry, Western blot methods and reverse transcription-PCR atprotein and mRNA levels in each group. The results showed that the degrees of fibrosis and histopathological damage of affected kidneys of mice in model group were the most obvious. And the expression levels of TLR4/MyD88 dependent signaling pathway-related molecules (TLR4 and MyD88, TRAF6 and NF-κB) in affected kidneys of mice in model group were the highest. At the same time, there was no difference in the expression levels of TLR4/MyD88 independent signaling pathway-related molecules（TRAM, TRIF）among sham-operated group, model group, astragaloside IV prevention group and astragaloside Ⅳ treatment group. In astragaloside Ⅳ prevention group and astragaloside Ⅳ treatment group, the injury of affected kidney was obviously reduced, and the protein expression levels of TLR4/MyD88 dependent signaling pathway-related molecules were also correspondingly reduced; at the same time, the expressions of terminal inflammatory cytokines (TNF-α,IL-6, IFN-) were suppressed. Therefore, astragaloside Ⅳ may improve renal interstitial fibrosis in mice after IRI by inhibiting the expression of TLR4/MyD88 dependent signaling pathway and the release of inflammatory cytokines (TNF-α,IL-6, IFN-), while the TLR4/MyD88 independent signaling pathway may not be involved in the process of renal fibrosis after ischemia-reperfusion injury.

A new oxoaporphine from Sabia limoniacea var. ardisioides / 药学学报

The chemical constituents of Sabia limoniacea var. ardisioides were investigated using chroma­tographic methods, such as silica gel, Sephadex LH-20 and preparative HPLC. Eight compounds were isolated and their structures were elucidated by spectral data and physicochemical properties, which were identified as 5-methoxy-1,2-methylenedioxyl oxoaporphine (1), fuseine (2), N-p-feruloyltyramine (3), N-trans-coumaroyl tyramin (4), quercetin (5), rutin (6), mutabiloside (7), and protocatechuic acid (8). Among those, compound 1 is a new compound, compounds 2−8 were isolated from this plant for the first time.

Identification of a novel HLA-A allele A*11:01:37 by sequence-based typing / 中华血液学杂志

<p><b>OBJECTIVE</b>To identify a novel HLA-A allele in a Chinese Han individual.</p><p><b>METHODS</b>One mismatch was observed in HLA-A locus in HLA typing for CMDP donors using bi-allelic SBT kit. A confirmatory test for novel HLA allele was performed with mono-allelic SBT kit.</p><p><b>RESULTS</b>The DNA sequence was confirmed to be a novel HLA-A allele. There was 1 nucleotide differed from the closest matching HLA-A*11:01:01 at position 393(G→A), which resulting a change from GGG to GGA at codon 107, led to a silent mutation, conserving the amino acid Gly.</p><p><b>CONCLUSION</b>A novel HLA-A allele was confirmed and officially named HLA-A*11:01:37 (Genbank accession number, JN209962) by the WHO Nomenclature Committee for Factors of the HLA System in January 2012.</p>

Value of quantitative examination via contrast-enhanced ultrasonography in evaluating the activity of Crohn disease at endoscopy / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To evaluate the predictive value of quantitative examination via contrast-enhanced ultrasonography on the activity of Crohn disease at endoscopy.</p><p><b>METHODS</b>A total of 59 cases with Crohn disease in People's Hospital of Lishui City between January 2009 and December 2010 were collected prospectively and underwent both colonoscopy and contrast-enhanced ultrasonography. According to the Simple Endoscopic Score, Crohn disease was divided into inactive and active disease by colonoscopy. To assess the vascularization of the involved bowel loop in a region expected to be seen at colonoscopy, the contrast agent uptake was measured by using quantitative analysis. Measurement of contrast enhancement was assessed as the percentage of increase in wall brightness in regions of interest (ROI). The receiver operating characteristic curve was used to evaluate the value of contrast agent uptake in predicting the severity determined at endoscopy.</p><p><b>RESULTS</b>Colonoscopy showed active lesions in 45 cases and inactive lesions in 14 cases, in whom the percentages of increase of brightness were (90±32)% and (41±29)% respectively. At a threshold value of 45% for the percentage of increase of brightness, sensitivity, specificity and accuracy of predicting the severity at endoscopy were 95.6%, 78.6% and 91.5%, the Youden index was 0.74, and area under curve was 0.846.</p><p><b>CONCLUSIONS</b>Quantitative measurement of bowel enhancement by using contrast-enhanced ultrasonography can discriminate between active and inactive Crohn disease at endoscopy. Contrast-enhanced ultrasonography may be a useful technique to monitor the activity of Crohn disease.</p>

The progressive effects of chronic intermittent hypoxia on cognitive function and the cholinergic neuron in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the relation between the progressive effects of chronic intermittent hypoxia (CIH) on cognitive function and the change of cholinergic neuron.</p><p><b>METHODS</b>Forty adult male Sprague-Dawley rats were randomly averagely divided into four groups: control group, CIH 1 week group, CIH 3 week group and CIH 5 week group. The cognitive function was assessed by the Morris Water Maze. The necrosis neurons in prefrontal cortex and hippocampus were observed and counted. The cholin acetyltransferase (ChAT) immunostained cells in prefrontal cortex and hippocampus were identified and quantitated.</p><p><b>RESULTS</b>The spatial learning and memory impairments progressed from 1 to 5 5 weeks in rats. Compared with the control group, the cognitive impairments in CIH5w group were significant (P < 0.05). The degeneration or necrosis neurons in prefrontal cortex and hippocampus were significantly increased in CIH rats, and worsen gradually along with the hypoxia. The ChAT immunostained cells in prefrontal cortex and hippocampus were gradually reduced. The ChAT immunostained cells of prefrontal cortex and hippocampus in CIH3w group and CIH5w group were less than that in control group (P < 0.05).</p><p><b>CONCLUSION</b>Chronic intermittent hypoxia induced slowly progressive spatial learning and memory impairments in rats, which maybe associated with the damage of neurons and the reduction of ChAT in prefrontal cortex and hippocampus.</p>