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1.
China Journal of Chinese Materia Medica ; (24): 596-602, 2018.
Article in Chinese | WPRIM | ID: wpr-771695

ABSTRACT

To explore the protective effect of naringin(Nar) on the injury of myocardium tissues induced by streptozotocin(STZ) in diabetic rats and the relationship with oxidative stress and endoplasmic reticulum stress(ERS), the male SD rats were intraperitoneally injected with streptozotocin(STZ, 60 mg·kg⁻¹) to establish the diabetic rat model and then randomly divided into the type 1 diabetic rat group(T1DR), the low-dose Nar group(Nar25), the middle-dose Nar group(Nar50) and the high-dose Nar group(Nar100). The normal rats were designed as control group(Con). Nar25, Nar50, Nar100 groups were orally administered with Nar at the doses of 25.0, 50.0, 100.0 mg·kg⁻¹ per day, respectively, while the normal group and the T1DR group were orally administered with saline. At the 8th week after treatment, fasting plasma glucose and heart mass index were measured. The pathological changes in myocardial tissues were observed by microscope. The cardiac malondialdehyde(MDA) level and superoxide dismutase(SOD) activities were measured. The gene and protein expressions of glucose-regulated protein 78(GRP78), C/EBP homologous protein(CHOP), cysteinyl aspartate-specific proteinase 12(caspase 12) were detected by qRT-PCR and Western blot. According to the results, compared with control group, the myocardial structure was damaged, the content of MDA was increased, while the activities of SOD were decreased(<0.05) in T1DR group. GRP78, CHOP and caspase 12 mRNA and protein expressions were increased significantly in T1DR group(<0.05, <0.01). Compared with T1DR group, myocardial structure damage was alleviated in Nar treatment group. The content of MDA was decreased, while the activities of SOD were increased significantly. The mRNA and protein expressions of GRP78, CHOP and caspase 12 were increased, especially in middle and high-dose groups(<0.05, <0.01). After treatment with Nar for 8 weeks, myocardial structure damage was obviously alleviated in Nar treatment groups. The content of MDA was decreased, while the activities of SOD were increased significantly in myocardial tissues. The mRNA and protein expressions of GRP78, CHOP and caspase 12 were increased, especially in middle and high-dose groups(<0.05, <0.01). The findings suggest that Nar may protect myocardium in diabetic rats by reducing mitochondrial oxidative stress injuries and inhibiting the ERS-mediated cell apoptosis pathway.


Subject(s)
Animals , Male , Rats , Apoptosis , Cardiotonic Agents , Pharmacology , Caspase 12 , Metabolism , Diabetes Mellitus, Experimental , Diabetic Cardiomyopathies , Drug Therapy , Endoplasmic Reticulum Stress , Flavanones , Pharmacology , Heat-Shock Proteins , Metabolism , Malondialdehyde , Metabolism , Oxidative Stress , Rats, Sprague-Dawley , Superoxide Dismutase , Metabolism , Transcription Factor CHOP , Metabolism
2.
Acta Academiae Medicinae Sinicae ; (6): 446-450, 2015.
Article in Chinese | WPRIM | ID: wpr-257613

ABSTRACT

<p><b>OBJECTIVE</b>To observe the morphology of hypertrophic scar tissue and explore the expressions and distribution of vascular endothelial growth factor (VEGF) and transforming growth factor beta activated kinase 1(TAK1 )in these tissues.</p><p><b>METHOD</b>Hematoxylin-eosin staining, Masson staining,immunofluorescence,and real-time polymerase chain reaction were used to detect the localization and expression of VEGF and TAK1 in 15 hypertrophic scar tissues and 10 normal skin tissues.</p><p><b>RESULTS</b>Morphological observation showed that the dermal fibroblasts in hypertrophic scar were disorderly and densely arranged (compared to the normal skin). Immunofluorescence displayed that the expressions of VEGF and TAK1 in hypertrophic scar tissue were higher than in normal skin tissues. Real-time polymerase chain reaction showed the mRNA expressions of both VEGF and TAK1 were significantly higher in hypertrophic scar tissue than in normal tissue (P<0.01, P<0.05,respectively).</p><p><b>CONCLUSIONS</b>Hypertrophic scar tissue has higher collagen fibrosis degree and higher TAK1 and VEGF expressions than the normal skin. VEGF and TAK1 can be used as the reference indicators for the diagnosis and differential diagnosis of hypertrophic scar and serve as new therapeutic targets.</p>


Subject(s)
Humans , Cell Shape , Cicatrix, Hypertrophic , Collagen , Fibroblasts , MAP Kinase Kinase Kinases , Transforming Growth Factor beta , Vascular Endothelial Growth Factor A
3.
Chinese Medical Journal ; (24): 2168-2172, 2012.
Article in English | WPRIM | ID: wpr-244393

ABSTRACT

<p><b>BACKGROUND</b>Serum testosterone levels have been found lower in acute ischemic stroke male patients. However, the exact mechanism remains unclear. In the present study, we measured serum testosterone levels, steroidogenesis- related genes and Leydig cells number in experimental transient cerebral ischemia male rats to elucidate the mechanism.</p><p><b>METHODS</b>The middle cerebral arteries of adult male Sprague-Dawley rats were sutured for 120 minutes and then sacrificed after 24 hours. Blood was collected for measurement of serum testosterone, follicular stimulating hormone and estradiol levels, and testes were collected for measurement of steroidogenesis-related gene mRNA levels and number of Leydig cells.</p><p><b>RESULTS</b>Serum testosterone levels in rats after cerebral ischemia were significantly lower (0.53 ± 0.16) ng/ml, n = 7, mean ± SE) compared with control ((2.33 ± 0.60) ng/ml, n = 7), while serum estradiol and follicular stimulating hormone levels did not change. The mRNA levels for luteinizing hormone receptor (Lhcgr), scavenger receptor class B member 1 (Scarb1), steroidogenic acute regulatory protein (StAR), cholesterol side chain cleavage enzyme (Cyp11a1), 3β-hydroxysteroid dehydrogenase 1 (HSD3β1), 17α-hydroxylase/20-lyase (Cyp17a1) and membrane receptor c-kit (kit) were significantly downregulated by cerebral ischemia, while luteinizing hormone, Kit ligand (KitL), 17β-hydrosteroid dehydrogenase 3 (HSD17β3) and 5α-reductase (Srd5a1) were not affected. We also observed that, relative to control, the Leydig cell number did not change.</p><p><b>CONCLUSIONS</b>These results indicate that transient cerebral ischemia in the brain results in lower expression levels of steroidogenesis-related genes and thus lower serum testosterone level. Transient cerebral ischemia did not lower the number of Leydig cells.</p>


Subject(s)
Animals , Male , Rats , Enzyme-Linked Immunosorbent Assay , Estradiol , Blood , Follicle Stimulating Hormone , Blood , Ischemic Attack, Transient , Blood , Metabolism , Leydig Cells , Metabolism , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Testis , Metabolism , Testosterone , Blood
4.
China Journal of Chinese Materia Medica ; (24): 1825-1827, 2008.
Article in Chinese | WPRIM | ID: wpr-252217

ABSTRACT

<p><b>OBJECTIVE</b>Using HPLC To determine hypoxanthine in co-hirudo injection for establishing its HPLC fingerprint, and evaluating its internal quality.</p><p><b>METHOD</b>The chromatographic separation was performed on a Kromasil C18 column (4.6 mm x 250 mm,5 microm). A linear gradient elution with A (0.01 mol x L(-1) x KH2PO4) and B (50% methanol) was used, the flow rate was 0.8 mL x min(-1), the detection wavelength was set at 254 nm, and the column temperature was at normal.</p><p><b>RESULT</b>Hypoxanthine was used as the reference substance in the fingerprint of co-hirudo injection, it showed 15 common peaks and theirs similarity threshod was 0.97.</p><p><b>CONCLUSION</b>This method was accurate, repeatable and useful for the quality control of co-hirudo injection.</p>


Subject(s)
Animals , Chromatography, High Pressure Liquid , Drugs, Chinese Herbal , Chemistry , Hypoxanthine , Chemistry , Leeches , Chemistry , Reproducibility of Results
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