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Taraxasterol augments 4-phenylbutyric acid inhibition of glucose-induced inflammation, cellular stress and mitochondrial dysfunction in HepG2 cellsTaraxasterol augments 4-phenylbutyric acid inhibition of glucose-induced inflammation, cellular stress and mitochondrial dysfunction in HepG2 cells

Olabisi Tajudeen Obafemi, Speaker at Traditional Medicine
University of South Africa, Johannesburg campus, South Africa
Title : Taraxasterol augments 4-phenylbutyric acid inhibition of glucose-induced inflammation, cellular stress and mitochondrial dysfunction in HepG2 cellsTaraxasterol augments 4-phenylbutyric acid inhibition of glucose-induced inflammation, cellular stress and mitochondrial dysfunction in HepG2 cells

Abstract:

Type 2 diabetes is characterized by hyperglycemia with associated mitochondrial dysfunction and cellular stress. 4-phenylbutyric acid (4PBA) is a chemical chaperone that ameliorates endoplasmic reticulum stress, while taraxasterol (TAX) is a pentacyclic triterpene whose antidiabetic potential is still being elucidated. The aims of this study are to evaluate the in vitro antidiabetic potentials in HepG2 cells, representing the liver, which is a glucose-utilizing organ. HepG2 cells were treated with high glucose concentration (40 mM), low TAX (25 μM), high TAX (50 μM), and 4PBA (2.5 mmol/L), for 24, 48 and 72 hours. Other groups contained glucose-treated cells that were also exposed to 4PBA, low TAX, high TAX, low TAX + 4PBA and high TAX + 4PBA. Colorimetric methods were used to determine the protein levels of antioxidant enzymes viz. superoxide dismutase (SOD) and catalase; inflammatory markers (interleukin-1β, and tumor necrosis factor alpha) and malondialdehyde. Real time polymerase chain reaction (RT-PCR) was used to estimate the mRNA levels of nuclear factor erythroid 2–related factor-2 (Nrf2) as well as endoplasmic reticulum (ER) stress markers - glucose regulated protein 78 (GRP78), activating transcription factor-4 (Atf4) and C/EBP homologous protein (CHOP). Mitochondrial dysfunction was evaluated by means of change in mitochondrial membrane potential. Results obtained from this study showed that both concentrations of TAX significantly (P < 0.05) increased the levels of antioxidant enzymes with a corresponding reduction of level of inflammatory proteins. Moreover, expression of ER stress markers was also significantly attenuated, while glucose-induced reduction of mitochondrial membrane potential was reversed. It was also observed that a synergy exists between TAX and 4PBA. It could be concluded that a synergistic effect between taraxasterol and 4-phenylbutyric acid inhibited glucose-induced cellular stress, inflammation and mitochondrial dysfunction in HepG2 cells.

Biography:

Dr Obafemi obtained a Ph.D in Applied Biochemistry at the Federal University of Technology Akure, Nigeria. He was an Academic Researcher at Afe Babalola University Ado-Ekiti, Nigeria, before joining University of South Africa in March 2024 as a Postdoctoral Researcher in the labs of Prof MM Ntwasa and Prof SL Lebelo. He conducts research on understanding the roles of mitochondrial dysfunction and endoplasmic reticulum stress in pathogenesis and progression of type 2 diabetes, and how they can be utilized as drug targets for diabetes therapies. He publishes his research in reputable peer-reviewed journals.

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