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1.
Biol Trace Elem Res ; 200(3): 1164-1170, 2022 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33860456

RESUMO

In this study, the effect of metformin on boron levels and oxidative brain damage in rats due to diabetes and prostate cancer was investigated for the first time. Myeloperoxidase (MPO) activity and the amount of DNA were investigated as tissue oxidative and toxic damage parameters. In Copenhagen rats, Dunning prostate cancer was induced using high metastatic MAT-Lylu cells and diabetes was induced by single dose of streptozotocin (STZ) injection. Metformin was administered for 14 days after diabetes and prostate cancer induced. The rats were divided into six groups as follows: control group, diabetic group (D), cancer group (C), diabetic + cancer (DC) group, cancer + metformin (CM) group, diabetic + cancer + metformin (DCM) group. At the end of the experiment, brains were removed. Significant decrease of brain boron levels and significant elevation of MPO activity and DNA levels were observed in D, C, and DC groups as compared to control group. The effect of diabetes induction on the brain boron levels was much more than prostate cancer induction. The administration of metformin with CM and DCM obviously declined MPO activity and increased brain boron levels almost near to control group level. In conclusion, this study shows that the protective effect of metformin against brain damage in STZ-induced diabetic rats with Dunning prostate cancer may also be related to increased boron levels. The boron levels may be a novel indicator of reduced toxic and oxidative stress. Furthermore, the distribution and mechanism of action of boron should be clarified.


Assuntos
Diabetes Mellitus Experimental , Metformina , Neoplasias da Próstata , Animais , Boro/farmacologia , Encéfalo , Diabetes Mellitus Experimental/tratamento farmacológico , Humanos , Hipoglicemiantes , Masculino , Metformina/farmacologia , Estresse Oxidativo , Peroxidase , Neoplasias da Próstata/tratamento farmacológico , Ratos , Estreptozocina
2.
J Food Biochem ; : e13835, 2021 Jun 26.
Artigo em Inglês | MEDLINE | ID: mdl-34173678

RESUMO

This study aimed to investigate the possible neuroprotective effects of bitter melon (BM), chard, and parsley extracts on oxidative damage that may occur in the brain of rats with bile duct ligation (BDL)-induced biliary cirrhosis. It was observed that lipid peroxidation (LPO), sialic acid (SA), and nitric oxide (NO) levels increased; glutathione (GSH) levels, catalase (CAT) activity, and tissue factor (TF) activity decreased significantly in the BDL group. However, in groups with BDL given BM, chard, and parsley extracts LPO, SA, NO levels decreased; GSH levels and CAT activities increased significantly. No significant differences were observed between groups in total protein, glutathione-S-transferase, superoxide dismutase, and boron. Histological findings were supported by the biochemical results. BM, chard, and parsley extracts were effective in the regression of oxidant damage caused by cirrhosis in the brain tissues. PRACTICAL APPLICATIONS: Bitter melon (BM), chard, and parsley have antioxidant properties due to their bioactive compounds which are involved in scavenging free radicals, suppressing their production, and stimulating the production of endogenous antioxidant compounds. Since BM, chard, and parsley extracts were found to be effective in the regression of oxidant damage caused by cirrhosis in the brain tissues, these plant extracts may be an alternative in the development of different treatment approaches against brain damage in cirrhosis. At the same time, these species have been used as food by the people for many years. Therefore, they can be used safely as neuroprotective agents in treatment.

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