Antioxidant Activity of Unripe Sapodilla Fruit Extract (Manilkara zapota L.) through Nrf2 and SOD Expression in Type 1 Diabetic Mice

Q4 Agricultural and Biological Sciences
F. Sari, R. Samoedra, S. Pratama, Sri Rahayu, A. Soewondo, M. Natsir, Muhaimin Rifa’i
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Abstract

This research aims to analyze the effect of unripe sapodilla fruit extract on endogenous antioxidant expression in T1DM BALB/c mice and its free radical scavenging activity. Manilkara zapota extract (MzE) is an aqueous extract of unripe sapodilla fruit and was obtained by maceration and freeze-drying process. This study used 25 male BALB/c mice with 7-weeks-old of age. They were divided randomly into five groups (n=5) before treatment. A single high dose (145 mg/kg BW) of streptozotocin (STZ) was intraperitoneally injected to induce type 1 diabetes mellitus (T1DM). MzE was given orally once each day for 14 days. Liver cells were isolated and immunoassay with anti-superoxide dismutase (SOD) and anti-nuclear factor erythroid 2-related Factor 2 (Nrf2), and then the results were analyzed by flow cytometry. Diphenylpicrylhydrazyl (DPPH) assay was performed to analyze free radical scavenging. Data were analyzed statistically with one-way ANOVA (p<0.05). The result showed that the glucose levels in diabetic mice after MzE administration were significantly lower than in the DM group. MzE treatment increased the expression of Nrf2 and SOD in diabetic mice. MzE could scavenge DPPH with the IC50 value obtained at 48.35 μg/mL, while ascorbic acid as a control could scavenge DPPH with the IC50 value at 22.24 μg/mL. The increase in the scavenging activity is in line with the increase in extract concentration. In conclusion, this study revealed that MzE can be an endogenous antioxidant enhancer by improving the expression of Nrf-2, SOD and can inhibit free radicals as an exogenous antioxidant in T1DM
1型糖尿病小鼠体内未成熟皂果提取物(Manilkara zapota L.)通过Nrf2和SOD表达的抗氧化活性
本研究旨在分析未成熟的皂荚果实提取物对T1DM BALB/c小鼠内源性抗氧化剂表达的影响及其清除自由基的活性。扎波塔碱提取物(MzE)是一种未成熟皂荚果实的水性提取物,通过浸渍和冷冻干燥工艺获得。本研究使用了25只7周龄的雄性BALB/c小鼠。在治疗前,他们被随机分为五组(n=5)。腹膜内注射单次高剂量(145mg/kg BW)链脲佐菌素(STZ)以诱导1型糖尿病(T1DM)。MzE每天口服一次,持续14天。用抗超氧化物歧化酶(SOD)和抗核因子红系2型相关因子2(Nrf2)分离肝细胞并进行免疫测定,然后用流式细胞术分析结果。用二苯基苦辛酰肼(DPPH)法分析自由基清除作用。数据用单因素方差分析进行统计学分析(p<0.05)。结果显示,糖尿病小鼠服用MzE后的血糖水平显著低于糖尿病组。MzE治疗增加了糖尿病小鼠Nrf2和SOD的表达。MzE可清除DPPH,IC50值为48.35μg/mL,抗坏血酸作为对照可清除DPPH,IC50为22.24μg/mL。清除活性的增加与提取物浓度的增加一致。总之,本研究表明MzE可以通过提高Nrf-2和SOD的表达而成为内源性抗氧化增强剂,并且可以作为外源性抗氧化剂抑制T1DM中的自由基
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Tropical Life Science
Journal of Tropical Life Science Environmental Science-Ecology
CiteScore
1.00
自引率
0.00%
发文量
46
审稿时长
12 weeks
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