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- Title
Silymarin promises hope for hyperglycemia treatment in HEPG2 cells.
- Authors
BEKTUR, Ezgi; KACAR, Sedat; SAHINTURK, Varol
- Abstract
Hyperglycemia is an abnormal condition, characterized by high glucose in bloodstream. Hyperglycemia causes several alterations in cell metabolism and signaling pathways. Silymarin is an herbal medicine, the antioxidant, anti-inflammatory properties of which were demonstrated in many studies (Crocenzi&Roma,2006). Therefore, we aimed at determining the effects of silymarin on hyperglycemiainduced HepG2 cells by examining the expression of NF-κβ and CPT1 proteins, closely associated with hyperglycemia (Ramana et al. 2004). In this regard, we divided the cells into 4 groups as control (only ready-to-use medium), mannitol (44.5 mM mannitol), hyperglycemia (50 mM glucose) and hyperglycemia+silymarin groups (50 mM glucose+25 μg/ml silymarin). The cells were exposed to respective media for 24 h. After 24 h, immunocytochemistry staining was implemented for NF-κβ and CPT1 proteins, and classical hematoxylin-eosin (HE) was applied for morphological evaluation of the cells. MDA levels were measured by colorimetric assay to determine ROS. As a result, NF-κβ and CPT1 immunoreactivity in mannitol group was comparable to control group. However, NF-κβ immunoreactivity and MDA levels increased but CPT1 immunoreactivity decreased in hyperglycemia group when compared to control. Silymarin treatment decreased NF-κβ, MDA levels and increased CPT1 expressions in the hyperglycemia+silymarin group. HE-stained cells were normal with euchromatic nuclei in control and mannitol groups, whereas degenerated cells with small and condensed nuclei were observed in hyperglycemia group. Silymarin treatment decreased these degenerative changes. In conclusion, 25 μg/ml of silymarin treatment ameliorated hyperglycemia-induced cellular degenerations by decreasing NF-κβ and increasing CPT1 expressions. Silymarin can be a promising agent for the treatment of hyperglycemia.
- Publication
Journal of Cellular Neuroscience & Oxidative Stress, 2018, Vol 10, Issue 2, p693
- ISSN
2149-7222
- Publication type
Academic Journal