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1.
Nutr Res ; 108: 22-32, 2022 Dec.
Article in English | MEDLINE | ID: mdl-36395709

ABSTRACT

Hyperglycemia is a symptom of type 2 diabetes mellitus, a chronic metabolic disease characterized by elevated blood glucose concentrations. Antidiabetic drugs are common treatments for this metabolic disorder; however, they may have unpleasant side effects. This study hypothesized that probiotic fermented products could preserve nutritional value, maintain metabolic homeostasis, and attenuate the inflammatory response associated with diabetes while reducing side effects. Lactobacillus plantarum KU985438 and Lactobacillus rhamnosus KU985439 showed the lowest alfa-amylase enzyme (α-amylase) activity among 8 lactobacilli tested. These 2 strains were used to develop functional fermented milk products, and their antidiabetic efficacy was tested in induced diabetic Wistar rats. The treatment of diabetic rats with L. plantarum KU985438 or L. rhamnosus KU985439 fermented yogurt resulted in a considerable reduction in blood glucose concentrations (136.79% and 145.17%, respectively) and α-amylase concentrations (56.84% and 56.84%, respectively) compared with conventional treatments. Diabetes relief began after 4 days of yogurt consumption compared with drug-based treatment. Significant improvements in both liver and kidney enzyme concentrations were also observed, in addition to a significant increase in high-density lipoprotein cholesterol concentrations and improved lipid profiles. Inhibition in nuclear factor κB and an increase in Bcl-2 concentrations were also detected. Histopathological examination of both hepatic and pancreatic cells revealed the positive effects of the studied treatment compared with standard treatment. Therefore, the selected Lactobacilli, which has hypoglycemic potential, could be used to produce functional nutraceutical antidiabetic supplements.


Subject(s)
Diabetes Mellitus, Experimental , Diabetes Mellitus, Type 2 , Lipid Metabolism Disorders , Probiotics , Rats , Animals , Hypoglycemic Agents/pharmacology , Hypoglycemic Agents/therapeutic use , Lactobacillus , Rats, Wistar , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/metabolism , Blood Glucose/metabolism , Diabetes Mellitus, Experimental/drug therapy , Yogurt , Lipid Metabolism Disorders/drug therapy , Anti-Inflammatory Agents/therapeutic use , alpha-Amylases
2.
Sci Rep ; 10(1): 10812, 2020 07 02.
Article in English | MEDLINE | ID: mdl-32616881

ABSTRACT

The purpose of this study is to investigate the therapeutic efficacy of individual or combined doses of dehydro-epiandrosterone (DHEA) and quercetin in ameliorating some biochemical indices in liver of CuO-NPs intoxicated-rats. CuO-NPs (50 nm) was administered as a daily oral dose 100 mg/kg for 2 weeks to rats followed by the fore-mentioned antioxidants for 1 month. We highlighted the therapeutic effect of DHEA and quercetin against CuO-NPs toxicity through monitoring the alteration of liver enzyme activity, antioxidant defense mechanism, necrosis, apoptosis, histopathological alterations, and DNA damage. The rats given CuO-NPs only showed marked significant elevation in liver enzymes, alteration in oxidant-antioxidant balance and an elevation in the hepatic inflammatory marker; tumor necrosis factor-α. Additionally, over expression of both caspase-3 and Bax proteins were detected. Whereas, Bcl2 was down regulated and DNA fragmentation was elevated. Moreover, Histopathological examination of hepatic tissue reinforced the previous biochemical results. Co-treatment with either DHEA, quercetin alone or in combination ameliorated the deviated parameters with variable degrees against CuO-NPs toxicity in rat. In conclusion, our findings suggested that the aforementioned treatments exert therapeutic effect in CuO-NPs toxicity by diminishing oxidative stress, mRNA gene expression and hepatic tissues DNA damage.


Subject(s)
Antioxidants/pharmacology , Antioxidants/therapeutic use , Apoptosis/drug effects , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/pathology , Dehydroepiandrosterone/pharmacology , Dehydroepiandrosterone/therapeutic use , Nanoparticles/toxicity , Oxidative Stress/drug effects , Oxidoreductases/toxicity , Quercetin/pharmacology , Quercetin/therapeutic use , Animals , Chemical and Drug Induced Liver Injury/drug therapy , DNA Damage/drug effects , DNA Fragmentation/drug effects , Drug Therapy, Combination , Liver/metabolism , Male , Proto-Oncogene Proteins c-bcl-2/metabolism , Rats, Wistar
3.
Toxicol Rep ; 6: 875-888, 2019.
Article in English | MEDLINE | ID: mdl-31516840

ABSTRACT

Alternative and complimentary usage of the natural compound has raised hopes of finding curative options for liver hepatocarcinogenesis. In the present study, the curative effect of bee honey against diethylnitrosamine (DEN) (50 mg/kg) and carbon tetrachloride (CCl4) (2 mg/Kg)-induced hepatocellular carcinoma (HCC) in male rats in the presence or absence of some chemotherapeutic drugs, Cisplatin (Cis), Cyclophosphamide (CY) and 5- Fluorouracil (5-FU) were investigated. The obtained results demonstrated that treatment with DEN/CCl4 caused oxidative stress as assigned by the increase in malondialdehyde (MDA) and fall in glutathione (GSH) content. Meantime detraction in the antioxidants, including superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST) and glutathione peroxidase (GPx) was observed. Also, the results showed induction of inflammation as reflected by an increase in the levels of both α- fetoprotein and α- fucosidase in the liver. This was accompanied by changes in the hepatic function biomarkers which characterized by the increased levels of transaminases (AST, ALT), alkaline phosphatase (ALP) and γ-Glutamyl transferase (γ-GT) and decrease in total protein content in the serum. In conclusion, the combination of the selected drugs and bee honey may be an effective chemo- preventive and therapeutic strategy for treating DEN and CCl4-induced HCC.

4.
World J Gastroenterol ; 18(44): 6379-86, 2012 Nov 28.
Article in English | MEDLINE | ID: mdl-23197883

ABSTRACT

The present study aims to clarify the protective effect of supplementation with some antioxidants, such as idebenone (200 mg/kg, ip), melatonin (10 mg/kg, ip) and arginine (200 mg/kg, ip) and their combination, on liver function (T. protein, albumin, alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase), energetic parameters (adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, inorganic phosphate, total adenylate, adenylate energy charge and potential phosphate). The effect on glycolytic and glycogenolytic enzymes (glucose, glycogen, glycogen phosphorylase, pyruvate kinase and phosphofructokinase against hypoxia) was also studied. The drugs were administered 24 and 1 h prior sodium nitrite intoxication. All biochemical parameters were estimated 1 h after sodium nitrite injection. Injection of sodium nitrite (75 mg/kg, sc) produced a significant disturbance in all biochemical parameters of liver function, energetic parameters and glycolytic and glycogenolytic enzymes. Hepatic damage was confirmed by histopathological examination of the liver as compared to controls. The marked changes in hepatic cells induced by sodium nitrite were completely abolished by pretreatment with the drug combination, suggesting potential protection against sodium nitrite-induced hypoxia. It could be concluded that a combination of both idebenone and melatonin or idebenone and arginine provides potential protection against sodium nitrite-induced hypoxia by improving biochemical parameters and preserving liver histology.


Subject(s)
Antioxidants/pharmacology , Chemical and Drug Induced Liver Injury/prevention & control , Dietary Supplements , Hypoxia/prevention & control , Liver/drug effects , Animals , Arginine/pharmacology , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/pathology , Cytoprotection , Disease Models, Animal , Drug Therapy, Combination , Energy Metabolism/drug effects , Hypoxia/chemically induced , Hypoxia/metabolism , Hypoxia/pathology , Liver/metabolism , Liver/pathology , Male , Melatonin/pharmacology , Oxidative Stress/drug effects , Rats , Reactive Oxygen Species/metabolism , Sodium Nitrite , Time Factors , Ubiquinone/analogs & derivatives , Ubiquinone/pharmacology
5.
Nat Prod Res ; 26(23): 2196-8, 2012.
Article in English | MEDLINE | ID: mdl-22103287

ABSTRACT

This research was performed to investigate in vitro the biological activities of successive as well as 70% ethanol extracts of Nepeta cataria on some biochemical parameters including oxidative markers and carbohydrate-hydrolysing enzyme activities (α-amylase, ß-galactosidase and α-glucosidase). Powdered N. cataria and its successive extracts were screened for their phytochemical constituents. Tests for tannins, carbohydrates, glycosides and flavonoids were positive in ethanolic extract, but those for steroids and terpenoids were positive in petroleum ether and chloroform extracts. Also, different extracts were chromatographically investigated. The results obtained demonstrated that different successive extracts of N. cataria exhibited an inhibitory effect on oxidative stress indices and carbohydrate-hydrolysing enzymes. It is observed that 70% ethanol, petroleum ether and chloroform extracts showed, respectively, the most potent inhibitory activities, while ethyl acetate and ethanol successive extracts appeared with moderate or low reducing activities.


Subject(s)
Enzyme Inhibitors/pharmacology , Nepeta/chemistry , Plant Extracts/chemistry , Plant Extracts/pharmacology , Antioxidants/chemistry , Antioxidants/pharmacology , Carbohydrate Metabolism , Carbohydrates/analysis , Chloroform/chemistry , Drug Evaluation, Preclinical/methods , Enzyme Inhibitors/chemistry , Ethanol/chemistry , Flavonoids/analysis , Free Radical Scavengers/pharmacology , Glycoside Hydrolase Inhibitors , Hydrolysis , Oxidative Stress/drug effects , Plant Extracts/analysis , Tannins/analysis , alpha-Amylases/antagonists & inhibitors , alpha-Amylases/metabolism , alpha-Glucosidases/metabolism , beta-Galactosidase/antagonists & inhibitors , beta-Galactosidase/metabolism
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