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1.
BMC Pregnancy Childbirth ; 23(1): 778, 2023 Nov 10.
Artigo em Inglês | MEDLINE | ID: mdl-37950229

RESUMO

OBJECTIVE: To investigate the expression of insulin-like growth factor binding protein-3(IGFBP-3) in HELLP syndrome and its possible role in the pathogenesis of this disease. METHODS: 1) 87 subjects were enrolled, including 29 patients with HELLP syndrome, 29 patients with pre-eclampsia (PE), and 29 healthy gravidae as control. The levels of IGFBP-3, IGF-1, TGF-ß1, and VEGF in maternal and umbilical blood of them were detected using ELISA. Correlation analysis was used to observe the correlation between IGFBP-3 and IGF-1/TGF-ß1/VEGF in maternal and umbilical blood, as well as that between maternal serum IGFBP-3 and clinical diagnostic indicators of HELLP syndrome. 2) Human hepatic sinusoid endothelial cells (HLSEC) and human umbilical vein endothelial cells (HUVEC) were cultured with different concentrations of IGFBP-3. After 72 h of culture, cell apoptosis and the normal living cells rate were detected and compared. RESULTS: 1) In both maternal and umbilical blood of HELLP group, levels of IGFBP-3 and TGF-ß1 were higher than control and PE group, IGF-1was lower than control group, VEGF was lower than control and PE group. IGFBP-3 in maternal blood was correlated with IGF-1/TGF-ß1/ VEGF, while IGFBP-3 in umbilical blood was linked to IGF-1/TGF-ß1. In maternal blood, there was a negative correlation between PLT and IGFBP-3, and a positive correlation between ALT/AST/LDH and IGFBP-3. 2) After cultured with IGFBP-3, the total apoptosis rate of either HLSEC or HUVEC was considerably elevated, while the normal living rate was decreased. CONCLUSION: The expression of IGFBP-3 is elevated in HELLP syndrome, which may subsequently promote cell apoptosis by affecting the expression and function of IGF-1, VEGF, and TGFß1 in the IGF/PI3K/Akt, TGF-ß1/Smad3, and VEGF/eNOS/NO pathways. IGFBP-3 aggravates inflammatory reactions of the vascular endothelium and liver under hypoxia, affects the normal function of cells, and plays a role in the pathogenesis of diseases.


Assuntos
Síndrome HELLP , Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina , Feminino , Humanos , Células Endoteliais/metabolismo , Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo , Fator de Crescimento Insulin-Like I/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Fator de Crescimento Transformador beta1 , Fator A de Crescimento do Endotélio Vascular
2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-257274

RESUMO

<p><b>OBJECTIVE</b>To assess Microcystin LR (MCLR)-induced acute toxic effects in male Sprague-Dawley rats.</p><p><b>METHODS</b>The rats were injected with MCLR intraperitoneally in different doses for different days. The organs and serum with rats were collected at 1 and 7 days after injection, and 7 days after the final injection (total 14 days). Pathological and enzymatic changes were observed.</p><p><b>RESULTS</b>The rats injected with 122 microg/kg MCLR showed myocardial cells damage including pyknosis, plasma dissolve and myofibrilla (pls check with dictionary) necrosis in the heart muscles after 24 hours. At the same time, the activities of serum glutamate-oxaloacetate transaminase (GOT), lactate dehydrogenase (LDH) and creatine phosphonase (CPK) were higher than these in the other groups (P < 0.01). The kidney was also damaged, kidney cell degeneration, and the increase of blood creatine (BCr) and blood urea nitrogen (BUN) were also seen. In liver pathological study, liver cell hemorrhage, degeneration and/or necrosis was observed. In serum the activities of glutamate-pyruvate transaminase (GPT), alkaline phosphatase (LDH) and GOT were higher than these in the other groups (P < 0.01).</p><p><b>CONCLUSION</b>These results suggested that MCLR can injure the heart, kidney and the liver in SD rats, and there is a dose-response relationship between MCLR and the toxic effect.</p>


Assuntos
Animais , Masculino , Ratos , Alanina Transaminase , Sangue , Aspartato Aminotransferases , Sangue , Nitrogênio da Ureia Sanguínea , Creatina , Sangue , Creatina Quinase , Sangue , Relação Dose-Resposta a Droga , Coração , Injeções Intraperitoneais , Rim , Patologia , L-Lactato Desidrogenase , Sangue , Fígado , Patologia , Toxinas Marinhas , Toxicidade , Microcistinas , Miocárdio , Patologia , Peptídeos Cíclicos , Toxicidade , Ratos Sprague-Dawley , Testes de Toxicidade Aguda
3.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-682452

RESUMO

Objective To study the expression of vascular endothelial growth factor(VEGF), microvessel density (MVD) and the relationship among angiogenesis,proliferation,and apoptosis in colorectal cancer (CRC). Methods Expression of VEGF mRNA was evaluated by semi quantitative RT PCR in 52 CRC samples and 48 adjacent normal colorectal tissue samples. The PCR product was sequenced to verify the desired results. Expressions of VEGF protein, MVD, proliferating index (PI), and apoptotic index (AI) were detected by immunohistochemical methods in 52 human CRC. Results Expression of VEGF mRNA was detected in a significantly greater proportion of colorectal carcinoma samples than that adjacent normal colorectal tissues (76.9% vs. 52.1%; P 0.05). The expression of VEGF protein was positively correlated with PI ( r =0.409, P 0.05). Conclusions VEGF may play an important role in the angiogenesis of colorectal carcinoma and cell proliferation, but may not directly correlate with cell apoptosis.

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