Curcumin Ameliorates Palmitic Acid-Induced Saos-2 Cell Apoptosis Via Inhibiting Oxidative Stress and Autophagy.

Baicheng Ma,Lei Yang,Gaopeng Guan,Qizhuang Lv,Youhua Xu

doi:10.1155/2021/5563660

Abstract

Objectives We aimed to determine the effects of curcumin on palmitic acid- (PA-) induced human osteoblast-like Saos-2 cell apoptosis and to explore the potential molecular mechanisms in vitro level. Methods Saos-2 cell were cultured with PA with or without curcumin, N-acetylcysteine (NAC, anti-oxidant), 3-methyladenine (3-MA, autophagy inhibitor) AY-22989 (autophagy agonist) or H2O2. Then, the effects of PA alone or combined with curcumin on viability, apoptosis, oxidative stress, and autophagy in were detected by CCK-8, flow cytometry assay and western blot. Results We found that autophagy was induced, oxidative stress was activated, and apoptosis was promoted in PA-induced Saos-2 cells. Curcumin inhibited PA-induced oxidative stress, autophagy, and apoptosis in Saos-2 cells. NAC successfully attenuated oxidative stress and apoptosis, and 3-MA attenuated oxidative stress and apoptosis in palmitate-induced Saos-2 cells. Interestingly, NAC inhibited PA-induced autophagy, but 3-MA had no obvious effects on oxidative stress in PA-treated Saos-2 cells. In addition, curcumin inhibited H2O2 (oxidative stress agonist)-induced oxidative stress, autophagy, and apoptosis, but curcumin had no obvious effect on AY-22989 (autophagy agonist)-induced autophagy and apoptosis. Conclusion The present study demonstrated that oxidative stress is an inducer of autophagy and that curcumin can attenuate excess autophagy and cell apoptosis by inhibiting oxidative stress in PA-induced Saos-2 cells.

Highlights

Diabetes mellitus is a pandemic metabolic disease and has a worldwide distribution
200 μM PA and 1.25–20 μM curcumin were added to the culture medium for 24 h to determine the effects of curcumin on palmitic acid- (PA-)induced Saos-2 cell viability. e results showed that 200 μM PA reduced cell viability by about 50%, and 1.25–10 μM curcumin prevented this reduction in cell viability in a dose-dependent manner
20 μM curcumin had no obvious effects on PAinduced cell apoptosis (Figure 1(c)). e colorimetric assay and western blot results showed that curcumin attenuated the expression of BAX and Caspase-3 but increased the expression of Bcl-2 in PA-treated Saos-2 cells (Figures 1(d) and 1(e))

Summary

Introduction

Diabetes mellitus is a pandemic metabolic disease and has a worldwide distribution. Diets rich in high-fat foods, especially saturated fats, are usually the cause of the clinical symptoms of metabolic syndrome, such as obesity, insulin resistance, and type 2 diabetes, which eventually increase the likelihood of osteoporosis [2]. Obesity and type 2 diabetes trigger a prolonged elevation of circulating free fatty acid levels (FFAs) especially the saturated FFAs such as palmitate (PA), which causes lipotoxicity in many cell types, including human osteoblast-like Saos-2 cell [3]. PA-induced lipotoxicity plays a vital role in the development and progression of osteoporosis [4, 5]. Numerous studies have focused on factors involved in the mechanism of PA-induced lipotoxicity, such as oxidative stress and autophagy [5]

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