A comparative evaluation of cardiac and neurological safety status of two commonly used oral hypoglycaemic agents in T2-DM Swiss albino mice model

Rahman, Md.; Ahmed, Shaheen; Mazumder, Tanoy; Salam, Md. Abdus; Baral, Prodip Kumar; Rana, Md Faruk; Mitra, Shuvo; Hossain, Sabbir; Rahman, Rubiya; Hussain, Md. Saddam

doi:10.1016/j.metop.2022.100191

Cited by 1 publication

(1 citation statement)

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“…The mice were raised at a temperature of 22 ± 2 °C and relative humidity of 60 ± 5% with a 12 h light/dark cycle. After adaptive feeding for seven days, all the mice were randomly divided into seven groups ( n = 10 in each group): the NC (normal control) group, the MC (model control) group, the PC1 (the first positive control, 200 mg·kg −1 metformin) group, the PC2 (the second positive control, 5 mg·kg −1 glimepiride) group, the EC30 (30 mg·kg −1 epimedin C) group, the EC10 (10 mg·kg −1 epimedin C) group, and the EC5 (5 mg·kg −1 epimedin C) group ( Table S1 ) [ 14 , 17 ]. Prior to oral administration (gavage) of different drugs (metformin, glimepiride, and epimedin C) or distilled water, the mice in the PC1, PC2, EC30, EC10, EC5, and MC groups were subjected to intraperitoneal injection of STZ with citrate buffer (pH 4.5).…”

Section: Methodsmentioning

confidence: 99%

The Mechanism Underlying the Hypoglycemic Effect of Epimedin C on Mice with Type 2 Diabetes Mellitus Based on Proteomic Analysis

Zhou,

Liu,

Yang

et al. 2023

Nutrients

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Type 2 diabetes mellitus (T2DM) has become a worldwide public health problem. Epimedin C is considered one of the most important flavonoids in Epimedium, a famous edible herb in China and Southeast Asia that is traditionally used in herbal medicine to treat diabetes. In the present study, the therapeutic potential of epimedin C against T2DM was ascertained using a mouse model, and the mechanism underlying the hypoglycemic activity of epimedin C was explored using a label-free proteomic technique for the first time. Levels of fasting blood glucose (FBG), homeostasis model assessment of insulin resistance (HOMA-IR), and oral glucose tolerance, as well as contents of malondialdehyde (MDA) and low-density lipoprotein cholesterol (LDL-C) in the 30 mg·kg−1 epimedin C group (EC30 group), were significantly lower than those in the model control group (MC group) (p < 0.05), while the contents of hepatic glycogen, insulin, and high-density lipoprotein cholesterol (HDL-C), as well as activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the EC30 group were notably higher than those in the MC group (p < 0.05). The structures of liver cells and tissues were greatly destroyed in the MC group, whereas the structures of cells and tissues were basically complete in the EC30 group, which were similar to those in the normal control group (NC group). A total of 92 differentially expressed proteins (DEPs) were enriched in the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. In the EC30 vs. MC groups, the expression level of cytosolic phosphoenolpyruvate carboxykinase (Pck1) was down-regulated, while the expression levels of group XIIB secretory phospholipase A2-like protein (Pla2g12b), apolipoprotein B-100 (Apob), and cytochrome P450 4A14 (Cyp4a14) were up-regulated. According to the KEGG pathway assay, Pck1 participated in the gluconeogenesis and insulin signaling pathways, and Pla2g12b, Apob, and Cyp4a14 were the key proteins in the fat digestion and fatty acid degradation pathways. Pck1, Pla2g12b, Apob, and Cyp4a14 seemed to play important roles in the prevention and treatment of T2DM. In summary, epimedin C inhibited Pck1 expression to maintain FBG at a relatively stable level, promoted Pla2g12b, Apob, and Cyp4a14 expressions to alleviate liver lipotoxicity, and protected liver tissues and cells from oxidant stress possibly by its phenolic hydroxyl groups.

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Section: Methodsmentioning

confidence: 99%