myricitrin and Hyperglycemia

The hyperglycemia (Hyper) induces oxidative stress in kidney tubular cells. Myricitrin (Myr) has an antioxidant effect along with low bioavailability.. The present research investigated the effects of Myr and its solid lipid nanoparticles (SLN) on isolated proximal tubules exposed to the hyperglycemic condition.. In this experimental study, the proximal tubules of mice were dissected by the microdissection method and the tubules were prepared for experimental or Real Time-PCR measurement.. The malondialdehyde level, transforming growth factor-β, nuclear factor kappa B and Bax genes expression increased in Hyper and decreased in Hyper + Myr and its SLN-treated groups compared to Hyper. Superoxide dismutase, total antioxidant capacity, the viability of proximal tubules and Bcl-2 gene expression decreased in untreated Hyper and increased in all treatment groups compared to Hyper.. The hyperglycemia-induced oxidative disorder, inflammation and apoptosis in proximal tubules and that administrating Myr and its SLN improved them.

Topics: Animals; Antioxidants; Flavonoids; Hyperglycemia; Liposomes; Mice; Nanoparticles; Oxidative Stress

Hyperglycemia induced oxidative stress inside the cells. Myricitrin, as an antioxidant plant-derived component, may be useful in hyperglycemia. Hence, the aim of this study was conducted to evaluate the antioxidant effects of myricitrin on hyperglycemia-induced oxidative damage in myotubes (C2C12 cells). In this experimental study, mouse myoblast cell line (C2C12) was obtained and divided into five groups: control, hyperglycemia, hyperglycemia + myricitrin 1, 3, and 10 μM. After treatment period for 48 h, cells were collected, homogenized, and centrifuged at 2000 rpm for 10 min. All samples were kept at - 80 °C until experimental and real-time PCR assessments were performed. Hyperglycemia increased malondialdehyde (MDA) (p < 0.05), total antioxidant capacity (TAC) (p < 0.001), and cellular apoptosis, and decreased levels of superoxide dismutase (SOD), catalase (CAT) (p < 0.01), myotube glycogen content (p < 0.05), glucose transporter type 4 (Glut-4), and cellular viability (p < 0.001). Myricitrin administration improved SOD (p < 0.05), CAT (p < 0.01), muscle cell's glycogen content (p < 0.01), Glut-4 gene expression (p < 0.001), Thiazolyl blue tetrazolium bromide (MTT) (p < 0.05), and Bax to Bcl-2 ratio (p < 0.001), and reduced MDA (p < 0.05) compared to hyperglycemia group. In conclusion, hyperglycemic condition induced oxidative stress along with cellular apoptosis, and myricitrin improved these disorders. Also, low and moderate doses of myricitrin are more efficient on skeletal muscle cells exposed to hyperglycemic statues than a high concentration of this antioxidant agent.

Topics: Animals; Antioxidants; Apoptosis; Cell Line; Cell Survival; Culture Media; Flavonoids; Gene Expression Regulation; Glucose; Glucose Transporter Type 4; Glycogen; Hyperglycemia; Lipid Peroxidation; Mice; Muscle Fibers, Skeletal; Oxidative Stress

Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.

Topics: Animals; Antioxidants; Apoptosis; Cell Line; Flavonoids; Glucose; Heme Oxygenase-1; Hyperglycemia; Mitochondria, Heart; Models, Biological; Myocytes, Cardiac; NF-E2-Related Factor 2; Oxidative Stress; Phosphatidylinositol 3-Kinases; Plant Extracts; Plants, Medicinal; Proto-Oncogene Proteins c-akt; Rats; Reactive Oxygen Species; Signal Transduction