Skip to main content
NCBI home page
Food Science and Biotechnology logoLink to Food Science and Biotechnology
. 2017 Dec 12;26(6):1703–1708. doi: 10.1007/s10068-017-0225-9

Antioxidant effect of peony seed oil on aging mice

Xiao-Miao Han 1, Su-Xi Wu 1,2,✉, Mei-Fang Wu 1, Xue-Feng Yang 3
PMCID: PMC6049733  PMID: 30263708

Abstract

d-galactose was injected into mice of ages 4–5 months, and peony seed oil was administered using an oral gavage to assess its possible anti-aging functions. The content of malondialdehyde (MDA) and the activities of monoamine oxidase (MAO), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the brain and liver of these mice were determined using biochemical kits. The significance of the differences in the content of the components associated with aging and anti-aging among each group was analyzed statistically. The MDA content and activities of MAO in the brain and liver of mice in the peony seed oil group were significantly lower than those in the aging group. The activities of GSH-Px, Cu/Zn-SOD, and Mn-SOD in the brain and liver of mice in the peony seed oil group were very significantly higher than those in the aging group. Peony seed oil was determined to have an obvious anti-aging function.

Keywords: Peony seed oil, Aging, Anti-aging, Superoxide dismutase

Introduction

Peony (Paeonia suffruticosa Andr.) is medicinal and ornamental plant. In China, it has been used for over 2000 years now. The medicinal part of peony is its dry root bark (Dan Pi), which promotes blood circulation and removes blood stasis, which is commonly performed when treating cardiovascular diseases, inflammations, allergies, and so on [1–4]. Seeds of peony are rich in oil [5, 6].

Peony seed oil is one of the functional foods that have been newly approved by the Chinese government. This oil’s content of polyunsaturated fatty acids exceeds 90%, and the content of linolenic acid is up to 40% [7–9]. Studies have shown that peony seed contains peony phenol; peony sterol; apigenin; trans-resveratrol; β-sitosterol; stigmasterol; suffruticosol A, B, C, and D; 8-debenzoylpaeonidanin; albiflorinR1; peoniflorin; nicotinic acid; vitamins E; caffic acid; oleanolic acid; and so on [10–13].

Recent studies have shown that peony seed oil is nontoxic and safe and has a very high nutritional value and many health benefits, including an antioxidant function, stimulation of blood circulation, lowering effect on blood glucose, prevention and treatment of diabetes mellitus, hepatoprotective effect, hypolipidemic effect, anti-UV and sunscreen effect, anti-tumor activity, antianaphylaxis, anti-inflammation, cardiovascular protection, anti-atherosclerosis, neuroprotective effect, reducing skin pigmentation, strengthening nonspecific immunity, relieving climacteric syndrome and rheumatoid arthritis, and so on [14–18]. Thus, peony seed oil is known as one of the “blood nutrients” and “plant brain gold” and has been processed into functional foods [19]. However, there is no systematic and in-depth research on the anti-aging effects of peony seed oil on aging animals.

During aging, the content of malondialdehyde (MDA) and the activity of monoamine oxidase (MAO) increase, whereas the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decrease. MDA can promote the formation of lipofuscin and the age pigment and accelerate aging. MAO can increase the breakdown of monoamine neurotransmitters, affect brain health, and promote aging. SOD and GSH-Px can accelerate the removal of free radicals and peroxides and delay senility [20–22]. Therefore, the content of MDA and the activities of MAO, SOD, and GSH-Px are important parameters for assessing the severity of body aging.

The aging animal model induced by d-galactose was integrated with the aging animal model design based on the principle of metabolic disturbance in the aging process [23–25]. In the animal body, d-galactose was reduced to galactitol by aldose reductase. The galactitol cannot be metabolized and accumulates in the cell, which can cause metabolic disturbance, Oxidative stress-free radical damage, the activity of antioxidant enzymes (SOD and GSH-Px) decreased, while the activity of MAO and the MDA content increased. On the other hand, d-galactose was transformed to advanced glycation end-products (AGEs) via nonenzymatic glycation. AGEs binding to the AGE receptor activated the signal pathway associated with AGEs, which can promote lipid peroxidation, strengthen the roles of the above-mentioned adverse effects on the body, and accelerate the aging of the organism. Each organ of the aging animal model exhibits different degrees of senility symptoms. Therefore, this aging model was an ideal experimental tool for studying the anti-aging effect and has been widely used to study the anti-aging action of drugs and functional foods [26–28].

To investigate the health effects of peony seed oil on aging mice, we administered the oil using an oral gavage to aging model mice induced by d-galactose and determined the components associated with aging and anti-aging.

Materials and methods

Materials

Fengdan peony seed oils were purchased from Shandong Heze Ruipu Peony Industry Technology Development Corporation, China.

Determination of peony seed oil dosage

Dong et al. [29] and Liu et al. [30] found that peony seed oil at a dose of 6 mL/kg body weight (BW)/day, significantly reduced the blood lipid content and had a significant antioxidant effect on hyperlipidemia mice. Based on these studies, we determined that peony seed oil dosage was 6 mL/kg BW/day.

Construction of the mouse model of the aging and anti-aging experiment

Following a 7-day acclimation period, 30 healthy male mice (Tianqing Biological Technology Co., Ltd, Changsha, China), 4–5 months of age and with BWs of 30 ± 5 g, were randomly assigned to 1 of three groups [1 peony seed oil group (PSOG), 1 aging model group (AMG), and 1 control group (CG)] comprising ten mice each. The mice were allowed free access to food and water. The experimental design was in accordance with the guidelines for animal experimentation. This experiment was approved by the Institutional Animal Care and Use Committee (IACUC) of the Changsha, China. (Changsha Tianqin Biotechnology Co., Ltd, approval number: Scxk (xiang) 2014-0011).

The basic feed (Tianqing Biological Technology, Changsha, China) constituted flour (20%), rice flour (10%), corn flour (20%), wheat bran (25%), bean (20%), bone meal (2%), and fish meal (2%).

The mice in the PSOG and in the AMG were subcutaneously injected with d-galactose (Sinopharm Chemical Reagent Co., Ltd, Shanghai, China) at a dose of 125 mg/kg BW/day [23–25] once daily for 6 weeks, whereas those in the CG were treated with the same volume (0.2 mL) of physiological saline. After injecting d-galactose, the mice in the PSOG were administered peony seed oil at a dose of 6 mL/kg BW/day using an oral gavage, whereas the mice in the AMG and the CG were administered the same volume of distilled water. Clinical observations were made following this treatment. The general conditions (appearance, behavior, dejecta, and temperament) and food consumption of all animals were recorded every day. The BWs of the mice were measured at commencement of the experiments and at the end of every other week.

Determination and analysis of components associated with aging and anti-aging

At the end of the sixth week, the animals were euthanized to undergo a gross pathological examination. The brain and liver were then removed from each cadaver. The brain and liver were homogenized (physiological saline = 1:9 for both) on ice according to the procedure described by Jin et al. [31], and the supernatant liquid of the homogenate was removed by centrifuging (1048×g) for 10 min for biochemical analysis (AqDL-5-8 centrifuge, Shanghai Xucheng Instrument Company, Shanghai, China). The content of MDA, the content of total protein (TP), and the activities of total-SOD (T-SOD), copper/zinc-SOD (Cu/Zn-SOD), GSH-Px, and MAO were determined using the appropriate biochemical analysis kit (Nanjing Jiancheng Bioengineering Institute, Nanjing, China) and the UV752N ultraviolet–visible spectrophotometer (Inesa Analytical Instrument, Shanghai, China) in accordance with the respective kit instructions. MAO activity was determined using a monoamine oxidase assay kit (Colorimetric method). MDA content was determined using a malondialdehyde assay kit (thiobarbituric acid test method). GSH-Px activity was determined using a glutathione peroxidase assay kit (colorimetric method). Content of TP was determined using a total protein quantitative assay kit. Activities of T-SOD and copper/zinc-SOD (Cu/Zn-SOD) were determined using a superoxide dismutase typed assay kit (hydroxylamine method). The activity of manganese-SOD (Mn-SOD) was obtained by subtracting the activity of Cu/Zn-SOD from that of T-SOD.

Statistical analysis

All data are expressed as mean ± SD. Statistical analysis was performed using one-way ANOVA and the Duncan test to explore the differences between groups (SPSS 16.0). Values having p < 0.05 were considered statistically significant.

Results and discussion

Appearance, behavior, dejecta, temperament, BW, and food consumption of mice

No mice died during the experiment. At the end of the testing period, the mice in the AMG exhibited obvious senility symptoms, such as reduced activity, sparse, dull yellow fur, irritable temperament, and thin dejecta. The appearance, behavior, dejecta, and temperament of mice in the PSOG were similar to those of the CG: they were in good condition; their temperament was mild; they displayed agility and nimbleness in their movements; their dejecta was normal; and their fur was thick and shiny (Table 1).

Table 1.

Comparison of appearance, behavior, dejecta, and temperament of mice in each group

Item AMG CG PSOG
Appearance Sparse dull yellow fur Thick and shiny fur Thick and shiny fur
Behavior Reduced activity Agility and nimbleness Agility and nimbleness
Ejecta Thin Normal Normal
Temperament Irritable Mild Mild
Open in a new tab

CG control group, AMG aging model group, PSOG peony seed oil group

A summary of the total BWs are presented in Table 2A. The results show that the BW gain of the mice in the AMG was significantly lower than that of the mice in the CG (p < 0.05) at the end of the experiment. By contrast, the BW gain of the mice in the PSOG was significantly higher than that of the mice in the CG (p < 0.05) and the AMG (p < 0.01).

Table 2.

Summary of the body weight data and food consumption values for mice in each group (n = 10)

Week 1 2 3 4 5 6
(A) Body weight data (g/mouse) Increased
 CG 34.49 ± 2.12 35.08 ± 3.71 35.23 ± 2.99 35.66 ± 3.32 36.15 ± 3.69 37.27 ± 3.68 2.44 ± 0.43
 AMG 32.51 ± 2.36 30.70 ± 2.80 31.05 ± 3.40 32.67 ± 3.67 32.88 ± 3.08 34.25 ± 3.04 1.07 ± 0.22*
 PSOG 34.63 ± 3.45 35.63 ± 3.58 35.91 ± 3.49 37.04 ± 3.17 36.65 ± 3.79 38.25 ± 3.02 3.52 ± 0.37*,##
(B) Food consumption values (g/day/mouse) Total (g/mouse)
 CG 5.00 ± 0.39 4.90 ± 0.80 4.94 ± 017 4.96 ± 0.83 4.78 ± 0.91 4.70 ± 0.64 204.98 ± 18.00
 AMG 3.73 ± 0.67 3.78 ± 0.45 4.50 ± 0.20 4.65 ± 0.24 4.62 ± 0.57 4.73 ± 0.32 182.16 ± 12.9*
 PSOG 4.13 ± 0.42 4.68 ± 0.62 4.96 ± 0.62 4.85 ± 0.64 4.51 ± 0.64 4.44 ± 0.73 192.66 ± 14.59
Open in a new tab

* p < 0.05 compared with the CG; ## p < 0.01 compared with AMG

The food consumption values are presented in Table 2B. The results show that the total food consumption values for mice in the AMG were significantly lower than those of mice in the CG (p < 0.05). The total food consumption values for mice in the PSOG were lower than those of the mice in the CG and higher than those of the mice in the AMG, but no significant difference was detected (p > 0.05).

Effect of peony seed oil on MDA content and MAO and GSH-Px activities

The MDA content and the activities of MAO and GSH-Px in the brain and liver of the mice in each group were determined using MDA, MAO, and GSH-Px kits, respectively. The results are shown in Table 3. The results showed that the MDA content and MAO activities in the brain and liver of the mice in the AMG were significantly (p < 0.05) or very significantly (p < 0.01) higher than those of the mice in the CG; however, the GSH-Px activities of mice in the AMG were significantly lower than those of mice in the CG (p < 0.05). The MDA content and MAO and GSH-Px activities in the brain and liver of mice in the PSOG did not significantly differ from those of the mice in the CG (p > 0.05) but significantly (p < 0.05) or very significantly (p < 0.01) differed from those of the mice in the AMG.

Table 3.

Comparison of MDA content and MAO and GSH-Px activities in the brain and liver of mice (n = 10)

Group MDA (nmol/mg prot) MAO (U/mg prot) GSH-Px (U/mg prot)
Brain Liver Brain Liver Brain Liver
CG 0.87 ± 0.10 1.58 ± 0.48 4.93 ± 0.78 2.31 ± 0.41 189.88 ± 19.88 449.50 ± 60.19
AMG 1.18 ± 0.29** 2.18 ± 0.56* 6.14 ± 0.82* 3.75 ± 0.59* 104.78 ± 7.92* 366.30 ± 57.85*
PSOG 0.90 ± 0.16## 1.59 ± 0.22# 5.05 ± 0.50# 2.43 ± 0.70# 156.81 ± 29.21# 430.16 ± 40.47##
Open in a new tab

** p < 0.01 and * p < 0.05 compared with the CG; ## p < 0.01; # p < 0.05 compared with AMG

Effect of peony seed oil on the activities of T-SOD, Cu/Zn-SOD, and Mn-SOD

The activities of T-SOD and Cu/Zn-SOD in the brain and liver of the mice in each group were determined using a SOD typed kit. The activity of Mn-SOD equals the activity of T-SOD minus the activity of Cu/Zn-SOD. The results are shown in Table 4. The results show that the activities of T-SOD, Cu/Zn-SOD, and Mn-SOD in the brain and liver of mice in the AMG were significantly lower than those of mice in the CG (p < 0.05). The activities of T-SOD, Cu/Zn-SOD, and Mn-SOD in the brain and liver of mice in the PSOG did not significantly differ from those of mice in the CG (p > 0.05) but were significantly higher than those of mice in the AMG (p < 0.05).

Table 4.

Comparison of the activities of T-SOD, Cu/Zn-SOD, and Mn-SOD in the brain and liver of mice (n = 10, U/mg prot)

Group T-SOD Cu/Zn-SOD Mn-SOD
Brain Liver Brain Liver Brain Liver
CG 219.37 ± 29.19 125.70 ± 13.61 164.87 ± 16.97 105.53 ± 8.75 54.50 ± 13.61 20.17 ± 10.61
AMG 157.25 ± 14.92* 98.97 ± 3.93* 120.77 ± 15.87* 87.38 ± 6.56* 36.48 ± 10.46* 11.59 ± 6.56*
PSOG 204.18 ± 33.29# 115.80 ± 9.03# 159.54 ± 30.03# 101.67 ± 4.82# 44.64 ± 9.78# 14.13 ± 9.78#
Open in a new tab

* p < 0.05 compared with the CG; # p < 0.05 compared with AMG

The results show that the mice in the AMG exhibited obvious senility symptoms. The MDA content and the activity of MAO in the brain and liver of the mice in the AMG significantly increased, and the activities of GSH-Px, T-SOD, Cu/Zn-SOD, and Mn-SOD significantly decreased.

The following findings demonstrated the remarkable anti-aging effects of peony seed oil:

  1. Peony seed oil contains many active ingredients, such as paeonol [17], paeoniflorin, and nicotinic acid [32] (see “Introduction” section). According to the fact that peony seeds can use their chemical components to develop and form vigorous seedlings, we considered that peony seed oil may also contain other active ingredients that can promote material transformation and metabolism and enhance the vitality of organisms. These active ingredients can remove blood stasis; stimulate blood circulation; promote body metabolism; accelerate the breakdown of sugars (d-galactose) and lipids; prevent formation and accumulation of galactitol, MDA, peroxides, and free radicals; reduce peroxidation; enhance the health of the body; and slow down the aging process.

  2. These active ingredients can enhance their anti-aging activities by repressing the expression of MAO and promoting expression of anti-oxidases GSH-Px, CuZn-SOD, and Mn-SOD [17, 33–35]. Studies have shown that a decrease in MAO content may reduce the breakdown of monoamine neurotransmitters, improve brain health, and prevent dementia [28, 29], while an increase in the anti-oxidase can accelerate the removal of free radicals and peroxides and delay aging [36–39].

  3. Peony seed oil contains large amounts of α-linolenic acid (up to 40%), which is an essential fatty acid. Research has shown that α-linolenic acid can derive many health care functions, such as inhibiting platelet aggregation, dilating blood vessels, improving blood circulation, and promoting the body’s metabolism, by transforming into prostacyclin, eicosapentaenoic acid, and docosahexaenoic acid in the body [40, 41].

  4. Peony seed oil contains many antioxidant components that can eliminate free radicals and peroxides through anti-oxidation, prevent lipid peroxidation and the subsequent formation of MDA, and reduce the MDA content in the brain and liver [19, 42].

Peony seed oil can significantly reduce the content or activity of components (such as MDA and MAO) that can cause aging, can significantly increase the activity of anti-oxidases (such as GSH-Px, Cu/Zn-SOD, and Mn-SOD) that have anti-aging functions, and can eliminate the aging effect of d-galactose in mice. Based on these findings, peony seed oil seems to have remarkable anti-aging effects.

Acknowledgements

This work was supported by the Research Fund for Science and Technology Project of Hunan Province in China (Grant No. 2016NK2136).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Contributor Information

Xiao-Miao Han, Phone: 008618229770323, Email: 1309926479@qq.com.

Su-Xi Wu, Phone: 008613469087959, Email: wusuxi@126.com.

Mei-Fang Wu, Phone: 008618390850244, Email: 964703693@qq.com.

Xue-Feng Yang, Phone: 008618390908602, Email: 2521486228@qq.com.

References

  • 1.Yang ZS, Peng ZH, Yao QH, Li Y. Advances in pharmacological effects of paeonol. Chin. Reme. Clin. 2011;11(5):545–547. [Google Scholar]
  • 2.Wu M, Gu Z. Screening of bioactive compounds from moutan cortex and their anti-inflammatory activities in rat synoviocytes. Evid. Based. Comple. Alternat. Med. 2009;6(1):57–63. doi: 10.1093/ecam/nem066. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Li YJ, Bao JX, Xu JW, Murad F, Bian K. Vascular dilation by paeonol—a mechanism study. Vascul. Pharmacol. 53(3–4): 169–176 (2010) [DOI] [PubMed]
  • 4.Li H, Dai M, Jia W. Paeonol attenuates high-fat-diet-inducedatherosclerosis in rabbits by anti-inflammatory activity. Planta. Med. 2009;75(1):7–11. doi: 10.1055/s-0028-1088332. [DOI] [PubMed] [Google Scholar]
  • 5.Dai HH, Wei AC, Li XD, Zhang LL. Research progress in the development and application of peony seed oil. Cereals. Oils. 2016;29(1):4–6. [Google Scholar]
  • 6.Zhang T, Gao TS, Bai RY, Huang XL, Guo N, Lu JX, Luo AC. Oil Peony Utilization and Research Progress. J. Chongqing. Normal. Univer. 2015;2:143–149. [Google Scholar]
  • 7.Zhu ZL, Wang FS, Mao WY. A New Resource of Food—Peony Seed Oil. Food. Drug. 2014;16:133–136. [Google Scholar]
  • 8.Qi JC, Zhou HM, Ma JQ, Li P. Analysis of the Chemical Constituents in Peony Seed Oil by GC-MS. Cereals. Oils. 2005;21:22–23. [Google Scholar]
  • 9.Mao CC, Li GH, Li PX, Zhu P, Kang XM. Analysis of Triglycerides Composition Structure and Physicochemical Properties of Peony Seed Oil. Mod. Food Sci. Techno. 2014;30:142–146. [Google Scholar]
  • 10.He CN, Xiao W, Li M, Peng Y, Xu LJ, Gu J, Xiao PG. Chemical Constituents from Seeds of Paenia Suffruticosa. Chin J. Chinese Materia Med. 2010;35(11):1428–1432. [PubMed] [Google Scholar]
  • 11.Yi JP, Zhu WX, Ma HL, Wang YF. Studies on Chemical Constituents from Seeds of Paeonia suffruticosa. Nat Prod Res Dev. 2009;21:604–607. [Google Scholar]
  • 12.Wu JY, Cao DL, Liu YC, Chang GP, Yu HP, Zhang HG. Chemical Constituents from Seed Meal of Paeonia Suffruticosa. Acta Chinese Med Pharmac. 2014;42:9–11. [Google Scholar]
  • 13.Li K, Zhou N, Li HY. Composition and Function Research of Peony Flowers and Peony Seeds. Food Res. Devel. 2012;33:228–230. [Google Scholar]
  • 14.Zhu WX, Li X, Liu SY, Bai X, Liu K. Toxicological Assessment of Peony Seed Oil. Food Sci. 2010;31:248–251. [Google Scholar]
  • 15.Qu WT, Zhu XB, Li YL, Xu H. Analysis of Composition and Antioxidant Activity in Peony Seed Oil. J. Yantai Univer. 2013;26:147–150. [Google Scholar]
  • 16.Zhu XB, Zhai WT, Dong XX, Xu H. Progress on chemical composition and function of peony seed oil. Chin Oils. Fats. 2014;39:88–90. [Google Scholar]
  • 17.Zhang JZ, Liu JC, Fan ZY, Chen LG, Luo JD. Exploration of Pathogenic Mechanism of Blood Stasis Syndrome. Associated with Essential Hypertension Through Investigating Effect of Paeonol on TLR-NF-κB Signal Pathway. J. Guangzhou Univer. Tradit. Chin Med. 2014;31:330–334. [Google Scholar]
  • 18.Sun SG, Liu J, Han YH, Song YF, Lu Y. Anxiolytic-like Effect of Active Phenolic Components from Moutan Cortex in Kunming Mice Animal Models. Chinese J. Exp. Tradit. Med. Formulae. 2013;19:283–287. [Google Scholar]
  • 19.Li H, Li C, Zhou YY, Li JL. Microencapsulation of Peony oil. Agr Sci. Tech. 2014;15:480–482. [Google Scholar]
  • 20.Chang YO, Kyung JL, Jae CL, Han SH. Differences of physiological injury and antioxidative reaction among three half-sib families of betula schmidtii to Cd treatment. J. Korean Fore Soc. 2004;93(7):428–435. [Google Scholar]
  • 21.Alvarez Garcia O, Vega-Naredo I, Sierra V, Caballero B. Elevated Oxidative Stress in the Brain of Senescence-accelerated Mice at 5 Months of age. Biogerontology. 2006;7:43–52. doi: 10.1007/s10522-005-6041-2. [DOI] [PubMed] [Google Scholar]
  • 22.Zhu LQ, Wang SH, Ling ZQ, Wang DL, Wang JZ. Effect of inhibiting melatonin biosynthesis on spatial memory retention and tau phosphorylation in rat. J. Pineal Res. 2004;37:71–77. doi: 10.1111/j.1600-079X.2004.00136.x. [DOI] [PubMed] [Google Scholar]
  • 23.Song X, Bao M, Li D, Li YM. Advanced glycation in d-galactose induced mouse aging model. Mechan. Ageing. Devel. 1999;108:239–251. doi: 10.1016/S0047-6374(99)00022-6. [DOI] [PubMed] [Google Scholar]
  • 24.Zhang X, Jiang B, Li Z, Hao S, An LJ. Catalpol ameliorates cognition deficits and attenuates oxidative damage in the brain of aging mice induced by d-galactose. Pharmacol. Biochem. Behav. 2007;88:64–72. doi: 10.1016/j.pbb.2007.07.004. [DOI] [PubMed] [Google Scholar]
  • 25.Wei HF, Li L, Song QJ, Ai HX, Chu J, Li W. Behavioural study of the d-galactose induced aging model in C57BL/6 J mice. Behav. Brain. Res. 2005;157:245–251. doi: 10.1016/j.bbr.2004.07.003. [DOI] [PubMed] [Google Scholar]
  • 26.Lu J, Zheng YL, Wu DM, Luo L, Sun DX, Shan Q. Ursolic acid ameliorates cognition deficits and attenuates oxidative damage in the brain of aging mice induced by d-galactose. Biochem Pharmacol. 2007;74:1078–1090. doi: 10.1016/j.bcp.2007.07.007. [DOI] [PubMed] [Google Scholar]
  • 27.Wang Y, Tao J. Anti-aging functions of a multi-vitamin on the mouse models aged by d-galactose. Food. Mach. 2012;26:64–66. [Google Scholar]
  • 28.Wang LM, Ye C, Wu C, Ma L, Liu ZG, Liu LJ. The effect of perilla oil on anti-aging for aging model rats. Food Sci. Tech. 2013;38:280–284. [Google Scholar]
  • 29.Dong ZX, Peng DY, Xun ZH, Liu CB. Experimental study on hypolipidemic and hypoglycemic effects of peony seed oil. Anhui Medical. Pharmaceutical. J. 2013;17:1286–1288. [Google Scholar]
  • 30.Liu CB, Xuan ZH, Dong ZX, Peng DY. Study on the Antioxidation Effect of Peony Seed Oil in Vitro and in Rats with Lipid Metabolism. J. Chin Cereals. Oils. Asso. 2014;29(6):53–56. [Google Scholar]
  • 31.Jin SL, Que F, Wang Y, Wei XX. Anti-aging effect of total polysaccharide from Dendranthema morifolium on aging mouse induced by d-galactose. Food Sci. Tech. 2015;36(10):349–351. [Google Scholar]
  • 32.Huang C. Beijing: People’s Health Press. Med. Nutr. 62 (2003)
  • 33.Benedetti SM, Dostert P. Monoamine oxidase, brain ageing and degenerative diseases. Biochem Pharm. 1989;38:555–561. doi: 10.1016/0006-2952(89)90198-6. [DOI] [PubMed] [Google Scholar]
  • 34.Lindley ES, She X, Schatzberg FA. Monoamine oxidase and catechol-o- methyltransferase enzyme activity and gene expression in response to sustained glucocorticoids. Psychoneuroendocrinology. 2005;30:785–790. doi: 10.1016/j.psyneuen.2005.03.007. [DOI] [PubMed] [Google Scholar]
  • 35.Li M, Zheng Y, Liang H, Zou L, Sun J, Zhang Y. Molecular cloning and characterization of cat, gpx1 and Cu/Zn-sod genes in pengze crucian carp (Carassius auratus var. Pengze) and antioxidant enzyme modulation induced by hexavalent chromium in juveniles. Comp. Biochem. Physio. Part C. 157: 310–321 (2013) [DOI] [PubMed]
  • 36.Lim H, Xie P, Zhang D, Chen J. The first study on the effects of microcystin-RR on gene expression profiles of antioxidant enzymes and heat shock protein-70 in Synechocystis sp. PCC6803. Toxicon. 2009;53:595–601. doi: 10.1016/j.toxicon.2008.11.005. [DOI] [PubMed] [Google Scholar]
  • 37.Pan M, Lai C, Tsai M, Wu J, Ho C. Molecular mechanisms for anti-aging by natural dietary compounds. Mol Nutr. Food Res. 2012;56:88–115. doi: 10.1002/mnfr.201100509. [DOI] [PubMed] [Google Scholar]
  • 38.Csire G, Demjen J, Timari S, Varnagy K. Electrochemical and SOD activity studies of copper(II) complexes of bis(imidazol-2-yl) derivatives. Polyhedron. 2013;61:202–212. doi: 10.1016/j.poly.2013.05.053. [DOI] [Google Scholar]
  • 39.Liu HH, He JY, Chi CF, Gu YF. Identification and analysis of icCu/Zn-SOD, Mn-SOD and ecCu/Zn-SOD in superoxide dismutase multigene family of Pseudosciaena crocea. Fish Shellfish Immun. 2015;43:491–501. doi: 10.1016/j.fsi.2015.01.032. [DOI] [PubMed] [Google Scholar]
  • 40.Wang HZ, Miao S, Sun JY. Progress of pharmacological research on alpha-lionolenic acid. Int. J. Pharm. Res. 2007;34:254–258. [Google Scholar]
  • 41.Tao HY, Li L, Chen JB, Tan XJ, Li SJ. Protective role of nano-α-linolenic acid on adriamycin-induced myocardium injury in rat and its mechanism. China. J. Mod. Med. 2006;16:1978–1982. [Google Scholar]
  • 42.Clarke MW, Burnett JR, Croft KD. Vitamin E in human health and disease. Cri. Rev. Clin Lab Sci. 2008;45:417–450. doi: 10.1080/10408360802118625. [DOI] [PubMed] [Google Scholar]

Articles from Food Science and Biotechnology are provided here courtesy of Springer

RESOURCES