Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Synthetic curcuminoid analogues abrogate oxidation-induced cell death and promote myogenic differentiation of C2C12 mouse myoblasts

Chittipong Tipbunjong¹ , Piyawat Sookbangnop², Vachiraporn Ajavakom³, Apichart Suksamrarn³, Yindee Kitiyanant⁴, Chumpol Pholpramool⁵

¹Department of Anatomy; ²Department of Biology, Faculty of Science, Prince of Songkla University, Songkhla 90112; ³Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Ramkhamhaeng University, Bangkok 10240; ⁴Department of Anatomy; ⁵Department of Physiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.

For correspondence:- Chittipong Tipbunjong Email: chittipong.t@psu.ac.th Tel:+66926345297

Accepted: 25 July 2018 Published: 31 August 2018

Citation: Tipbunjong C, Sookbangnop P, Ajavakom V, Suksamrarn A, Kitiyanant Y, Pholpramool C. Synthetic curcuminoid analogues abrogate oxidation-induced cell death and promote myogenic differentiation of C2C12 mouse myoblasts. Trop J Pharm Res 2018; 17(8):1483-1489 doi: 10.4314/tjpr.v17i8.4

© 2018 The authors.
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Abstract

Purpose: To investigate the ability of two synthetic curcuminoid analogues, 6-(4-hydroxy-3-methoxyphenethyl)-5-(3-(4-hydroxy-3-methoxyphenyl)propanoyl)-4-phenyl-3,4-dihydropyrimidin-2(1H)-one (compound A) and 6-(4-hydroxy-3-methoxyphenethyl)-4-(4-hydroxy-3-methoxyphenyl)-5-(3-(4-hydroxy-3-methoxyphenyl)propanoyl)-3,4-dihydropyrimidin-2(1H)-one (compound B), to protect against oxidation-induced cell death and the potential to enhance proliferation and differentiation of C2C12 myoblast cells.

Methods: Antioxidant activity of curcuminoid analogues was evaluated by DPPH assay. The cytotoxic activity of the compounds (0 - 25 mM) on C2C12 myoblasts was determined by MTT assay while the effect on cell proliferation was assessed by BrdU uptake. Myoblast cell differentiation was measured by the formation of myotubes and myosin heavy chain (MHC) protein expression using immunofluorescence staining and Western blotting, respectively.

Results: Both curcuminoid analogues exhibited strong anti-oxidant activity of up to 3-fold greater than that of ascorbic acid, and were non-toxic to C2C12 myoblasts at concentrations up to 25 mM. Furthermore, these curcuminoid analogues mitigated myoblast cell death induced by oxidative stress. Notably, both analogues (10 nM) had no effect on cell proliferation. However, only compound A significantly enhanced myoblast differentiation comparable to the effects of dihydrotestosterone (1 µM) and estradiol (10 nM).

Conclusion: The results suggest that compound A may serve as a lead compound for the development of suitable therapeutic agents for muscle injuries and diseases.

Keywords: Curcuminoid analogues, Antioxidant, Cell proliferation, Cell differentiation, Myoblasts