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1.
Stud Health Technol Inform ; 308: 105-110, 2023 Nov 23.
Artigo em Inglês | MEDLINE | ID: mdl-38007731

RESUMO

Aflatoxin is a highly toxic substance, of which aflatoxin B1 is the most toxic and carcinogenic among aflatoxins. In this paper, the team used homemade CdSe/Zns quantum dots to construct a fluorescent immunoprobe and all-antigen coupling with aflatoxin B1. It used a self-developed fluorescence intensity detector to detect aflatoxin B1 in five traditional Chinese medicines, namely, ginseng, Panax ginseng, Chuanxiong rhizome, rhubarb, and yam. The recoveries were 80.0-102.0%; the relative standard deviations (RSD)were from 2.4 to 9.2.


Assuntos
Compostos de Cádmio , Pontos Quânticos , Compostos de Selênio , Aflatoxina B1/análise , Fluorescência
2.
Appl Physiol Nutr Metab ; 42(10): 1015-1022, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28575637

RESUMO

Atherosclerosis is a chronic disease that can seriously endanger human life. Folic acid supplementation modulates several disorders, including atherosclerosis, via its antiapoptotic and antioxidative properties. This study investigated whether folic acid alleviates atherogenesis by restoring homocysteine levels and antioxidative capacity in atherosclerosis Wistar rats. To this end, 28 Wistar rats were randomly divided into 4 groups (7 rats/group) as follows: (i) wild-type group, fed only the AIN-93 semi-purified rodent diet (folic acid: 2.1 mg/kg); (ii) high-fat + folic acid-deficient group (HF+DEF) (folic acid: 0.2 mg/kg); (iii) high-fat + normal folic acid group (folic acid: 2.1 mg/kg); and (iv) high-fat + folic acid-supplemented group (folic acid: 4.2 mg/kg). After 12 weeks, histopathological changes in the atherosclerotic lesions of the aortic arch were determined. In addition, serum folate levels, plasma homocysteine levels, plasma S-adenosyl-homocysteine levels, antioxidant status, oxidant status, and lipid profiles were evaluated. The results show aggravated atherosclerotic lesions in the HF+DEF group. Folic acid supplementation increased concentrations of serum folate. Further, folic acid supplementation increased high-density lipoprotein-cholesterol, decreased plasma homocysteine levels, and improved antioxidant capacity in atherogenic rats. These findings are consistent with the hypothesis that folic acid alleviates atherogenesis by reducing plasma homocysteine levels and improving antioxidant capacity in rats fed a high-fat diet.


Assuntos
Antioxidantes/farmacologia , Aorta Torácica/efeitos dos fármacos , Doenças da Aorta/prevenção & controle , Aterosclerose/prevenção & controle , Ácido Fólico/farmacologia , Homocisteína/sangue , Estresse Oxidativo/efeitos dos fármacos , Animais , Antioxidantes/metabolismo , Aorta Torácica/metabolismo , Aorta Torácica/patologia , Doenças da Aorta/sangue , Doenças da Aorta/patologia , Aterosclerose/sangue , Aterosclerose/patologia , HDL-Colesterol/sangue , Dieta Hiperlipídica , Modelos Animais de Doenças , Ácido Fólico/sangue , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Placa Aterosclerótica , Ratos Wistar , Fatores de Tempo
3.
Int J Mol Sci ; 18(5)2017 May 05.
Artigo em Inglês | MEDLINE | ID: mdl-28475147

RESUMO

The pathogenesis of atherosclerosis has been partly acknowledged to result from aberrant epigenetic mechanisms. Accordingly, low folate levels are considered to be a contributing factor to promoting vascular disease because of deregulation of DNA methylation. We hypothesized that increasing the levels of folic acid may act via an epigenetic gene silencing mechanism to ameliorate atherosclerosis. Here, we investigated the atheroprotective effects of folic acid and the resultant methylation status in high-fat diet-fed ApoE knockout mice and in oxidized low-density lipoprotein-treated human umbilical vein endothelial cells. We analyzed atherosclerotic lesion histology, folate concentration, homocysteine concentration, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), and DNA methyltransferase activity, as well as monocyte chemotactic protein-1 (MCP1) and vascular endothelial growth factor (VEGF) expression and promoter methylation. Folic acid reduced atherosclerotic lesion size in ApoE knockout mice. The underlying folic acid protective mechanism appears to operate through regulating the normal homocysteine state, upregulating the SAM: SAH ratio, elevating DNA methyltransferase activity and expression, altering MCP1 and VEGF promoter methylation, and inhibiting MCP1 and VEGF expression. We conclude that folic acid supplementation effectively prevented atherosclerosis by modifying DNA methylation through the methionine cycle, improving DNA methyltransferase activity and expression, and thus changing the expression of atherosclerosis-related genes.


Assuntos
Quimiocina CCL2/genética , Metilação de DNA , Ácido Fólico/uso terapêutico , Placa Aterosclerótica/tratamento farmacológico , Fator A de Crescimento do Endotélio Vascular/genética , Complexo Vitamínico B/uso terapêutico , Animais , Apolipoproteínas E/genética , Suplementos Nutricionais , Ácido Fólico/administração & dosagem , Ácido Fólico/farmacologia , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Placa Aterosclerótica/genética , Placa Aterosclerótica/metabolismo , Placa Aterosclerótica/prevenção & controle , Regiões Promotoras Genéticas , S-Adenosil-Homocisteína/metabolismo , S-Adenosilmetionina/metabolismo , Complexo Vitamínico B/administração & dosagem , Complexo Vitamínico B/farmacologia
4.
Exp Ther Med ; 5(3): 695-700, 2013 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-23408474

RESUMO

To investigate the effects of Hu Qisan (HQS) on apoptosis in diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC), a Solt-Farber two-step test model of precancerous liver lesions was established in rats using a previously described method. HQS (4 and 8 g/kg body weight/day) was administered for 4 weeks, after the majority of the liver was removed. HepG2 cells were used to detect the HtrA serine peptidase 2 (HtrA2/Omi) release from mitochondria and caspase-3 activation promoted by HQS. Exposure of the rats to DEN for 6 weeks induced hepatic carcinogenesis. HQS (4 and 8 g/kg body weight/day) markedly induced cell apoptosis. The protective effects against hepatic carcinogenesis were mediated by multiple mechanisms, including the reduction of DEN-induced γ-GT-positive cell proliferation, mitochondrial morphological changes, HtrA2/Omi release from mitochondria and the activation of caspase-3. In conclusion, HQS is a potential anti-carcinogenic agent that may induce apoptosis by reducing the inhibitory effects of X-linked inhibitor of apoptosis protein (XIAP) on caspase-3. Thus, HQS should be further explored as a potentially promising new therapeutic agent against human hepatic cancer.

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