RÉSUMÉ
Objective:To investigate the relationship between serum lipids and Parkinson's disease, and its predictive value for Parkinson's disease. Methods:From January, 2016 to November, 2018, 145 patients with Parkinson's disease and other 122 healthy subjects were selected. They were measured the various lipid indexes. Results:Total cholesterol, low density lipoprotein cholesterol, Apolipoprotein A1 (ApoA1) and Apolipoprotein B (ApoB) were less in the patients than in the controls (t > 2.089, P < 0.05). ApoA1 was an independent protective factor from Logistic regression (OR = 0.081, P < 0.01). The most optimal cut-off threshold of ApoA1 was 1.38 mmol/L, with the sensitivity of 0.72 and the specificity of 0.68. Conclusion:The lipid decreased in patients with Parkinson's disease. Low ApoA1 may be a potential independent risk factor for Parkinson's disease, which may be a predictor for it.
RÉSUMÉ
<p><b>OBJECTIVE</b>To observe the effect of platelet-rich plasma (PRP) on the proliferation and adipogenic differentiation of human adipose-derived stem cells in vitro.</p><p><b>METHODS</b>Human adipose-derived stem cells were obtained by enzymatic digestion and PRP was prepared by dual centrifugal method. The ADSCS were interfused with 5%, 10%, and 20% PRP in conditioned culture media, using the untreated cells as the control group. The morphology of the cells were observed and their proliferative ability was detected using XTT colorimetric assay. The adipogenic differentiation ability of the cells was evaluated using oil Red O staining.</p><p><b>RESULTS</b>The ADSCS treated with PRP showed better morphology with higher density than the control cells. XTT colorimetric assay demonstrated obviously stronger proliferative activity of PRP-treated cells than the control group (P<0.01). Interfusion with PRP caused a significant increase in adipogenic differentiation of the cells as compared to the control cells (P<0.01).</p><p><b>CONCLUSION</b>PRP treatment produces obvious effects on the proliferation and adipogenic differentiation of human adipose-derived stem cells in vitro.</p>
Sujet(s)
Humains , Adipocytes , Biologie cellulaire , Tissu adipeux , Biologie cellulaire , Techniques de culture cellulaire , Différenciation cellulaire , Prolifération cellulaire , Cellules cultivées , Milieux de culture conditionnés , Lipectomie , Plasma riche en plaquettes , Cellules souches , Biologie cellulaire , Ingénierie tissulaire , MéthodesRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the effect of irbesartan on the renal expressions of advanced glycation end products (AGEs) and their receptor (RAGEs) in rats with early diabetic nephropathy (DN) and the renoprotection mechanism of irbesartan.</p><p><b>METHODS</b>Rat DN models established by a single injection of streptozotocin were randomly divided into the model group and irbesartan treatment group. With normal rats as the control, all the rats received daily gavage for 8 weeks. The 24-h urinary protein excretion and contents of AGEs in the serum and kidney tissues were measured. The expressions of RAGEs and RAGEs protein and mRNA in the kidney tissues were detected by immunohistochemistry and reverse transcription-polymerase chain reaction, respectively. The pathological changes of the kidney were also assessed microscopically.</p><p><b>RESULTS</b>Irbesartan significantly reduced the 24-h urinary protein excretion and the contents of AGEs in the serum and kidney tissues of DN rats, resulting also in decreased expressions of RAGEs and RAGEs protein and mRNA levels in the kidney. The treatment obviously alleviated the pathological changes in the kidney of the DN rats.</p><p><b>CONCLUSION</b>Irbesartan offers renoprotection against DN possibly by reducing the serum and renal contents of AGEs and inhibiting the renal mRNA expressions of RAGEs and RAGEs.</p>
Sujet(s)
Animaux , Mâle , Rats , Antagonistes du récepteur de type 1 de l'angiotensine-II , Utilisations thérapeutiques , Dérivés du biphényle , Utilisations thérapeutiques , Diabète expérimental , Néphropathies diabétiques , Traitement médicamenteux , Métabolisme , Produits terminaux de glycation avancée , Génétique , Métabolisme , Rein , Métabolisme , ARN messager , Génétique , Métabolisme , Répartition aléatoire , Rat Sprague-Dawley , Récepteur spécifique des produits finaux de glycosylation avancée , Récepteurs immunologiques , Génétique , Métabolisme , Tétrazoles , Utilisations thérapeutiquesRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the morphological changes and expressions of desmin and podocin in podocytes of rats with diabetic nephropathy (DN) rats and renal protection mechanism of Shenkangwan.</p><p><b>METHODS</b>DN model was established in rats by a single injection of streptozotocin. The rats were then randomly divided into model group, Shenkangwan treatment group, irbesartan treatment group, and Shenkangwan plus irbesartan treatment group, with normal rats as the control group. All the rats received daily gavage for 8 weeks. The urinary protein quantity in 24 h were detected, and the morphological changes of the kidneys were observed with optic and transmission electron microscopes. The expressions of desmin and podocin in the podocytes were detected by immunohistochemistry.</p><p><b>RESULTS</b>Shenkangwan and irbesartan reduced the urinary protein quantity in 24 h and alleviated the renal damage in DN rats, and the expression of desmin was significantly attenuated while podocin expression increased in the podocytes.</p><p><b>CONCLUSIONS</b>Shenkangwan can provide renal protection against DN in rats and alleviate the structural and functional damages of podocytes possibly by reducing desmin expression and increasing podocin expression in the podocytes.</p>
Sujet(s)
Animaux , Mâle , Rats , Desmine , Néphropathies diabétiques , Traitement médicamenteux , Anatomopathologie , Médicaments issus de plantes chinoises , Pharmacologie , Utilisations thérapeutiques , Immunohistochimie , Rein , Anatomopathologie , Microscopie électronique à transmission , Phytothérapie , Podocytes , Métabolisme , Anatomopathologie , Répartition aléatoire , Rat Sprague-DawleyRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the effect of 5F from Pteris semipinnate L on the growth of human pathological scar in nude mice.</p><p><b>METHODS</b>5F from Pteris semipinnate L was administered at different doses in nude mouse models bearing human pathological scars. The morphology, histology, tumor growth factor-beta1 and type I collagen content of the scar tissues were examined after the administration.</p><p><b>RESULTS</b>Administration of 5F significantly reduced the volume of the implanted pathological scars in the nude mouse models, and histologically, the scar tissue exhibited a transition to the normal scar architecture with decreased TGF-beta1 and type I collagen content.</p><p><b>CONCLUSION</b>5F could effectively inhibit the growth of pathological scars in nude mice.</p>