• Title/Summary/Keyword: Anti-Lipid Peroxidation

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Beneficial Effects of Acanthopanax senticosus Extract in Type II Diabetes Animal Model via Down-Regulation of Advanced Glycated Hemoglobin and Glycosylation End Products (제2형 당뇨 동물모델에서 가시오가피 추출물의 당화혈색소 및 최종당화산물 억제를 통한 혈당조절 효과)

  • Kwon, Han Ol;Lee, Minhee;Kim, Yong Jae;Kim, Eun;Kim, Ok-Kyung
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.45 no.7
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    • pp.929-937
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    • 2016
  • The purpose of this study was to investigate the effect of Acanthopanax senticosus extract (ASE) (ethanol : DW=1:1, v/v) on inhibition of type 2 diabetes using an OLETF rat model via regulation of HbA1c and AGEs levels. Supplementation with ASE 0.1% and 0.5% effectively lowered levels of glucose, insulin, oral glucose tolerance test, and Homa-insulin resistance, suggesting reduced insulin resistance. Blood levels of HbA1c and AGEs were significantly reduced in a dose-dependent manner. As oxidative stress plays a key role in accelerating production of HbA1c and AGEs, which worsen symptoms of type 2 diabetes, levels of malonaldehyde and pro-inflammatory cytokines were measured. Lipid peroxidation in both blood and liver tissues was significantly reduced, and induction of pro-inflammatory cytokines interleukin-${\beta}$ and tumor necrosis factor-${\alpha}$, which elevate production of HbA1c and AGEs, was inhibited (P<0.05). To evaluate the possible cellular events after AGEs receptor activation, genetic expression of protein kinase C (PKC)-${\delta}$ and transforming growth factor (TGF)-${\beta}$ was measured by real-time polymerase chain reaction. Supplementation with both ASE 0.1% and 0.5% significantly inhibited mRNA expression of PKC-${\delta}$ and TGF-${\beta}$, indicating that ASE may have beneficial effects on preventing insulin-resistant cells or tissues from progressing to diabetic complications. Taken together, ASE has potential to improve type 2 diabetes by inhibiting insulin resistance and protein glycosylation, including production of HbA1c and AGEs. Anti-oxidative activities of ASE are a main requisite for reducing production of HbA1c and AGEs and are also related to regulation of the PKC signaling pathway, resulting in suppression of TGF-${\beta}$, which increases synthesis of collagen, prostaglandin, and disease-related proteins.

The Protective Effect of Orally Ingested Korean Red Ginseng on the Noise Induced Hearing Loss in Mice (마우스에서 고려 홍삼의 구강내 섭취를 통한 소음성 난청의 예방효과)

  • Ahn, Joong-Ho;Kim, Tae-Soo;Chung, Hana;Lee, Na-Young;Chung, Jong-Woo
    • Journal of Ginseng Research
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    • v.33 no.2
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    • pp.104-110
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    • 2009
  • It is well known that the saponin of Korean red ginseng (KRG) has an anti-oxidant effect and could suppress the accumulation of lipid peroxidation. The aim of the present study was to observe the inhibitory effect of KRG on mice with noise-induced hearing loss, and to determine its optimal dose. BALB/c mice with a normal hearing level and normal Preyer's reflexes were used in the study. The mice in the permanent-threshold-shift (PTS) group were exposed to noise (120-dB SPL, white noise band) in a noise booth for 3 h a day, for three consecutive days. The mice in the experimental group were given heat-processed red-ginseng extract (50 mg/kg, 100 mg/kg, and 200 mg/kg), and those in the control group were given normal saline alone during their noise exposure. The mice in the temporary-threshold-shift (TTS) group were exposed to noise (120 dBSPL, white noise band) in a noise booth for 3 h. The mice in the experimental group were given heat-processed red-ginseng extract (50 mg/kg, 100 mg/kg, and 200 mg/kg), and those in the control group were given normal saline alone before their noise exposure. The hearing levels of the mice were measured through auditory brainstem response (ABR) immediately and I, 3, 5, 7, and 14 days after their noise exposure. Cochleae were removed from the mice 14 days after their noise exposure. lmmunochemical and immunofluorescent staining were performed to observe the expression of 8-oxoG in cochlea. In the PTS group, the hearing function of the mice in all the groups was not recovered after their noise exposure. In the TTS group, however, the hearing function of the mice in all the groups was recovered within 14 days. Reduced hearing impairment and early recovery were observed in the mice that were given 200 mg/kg KRG, and early recovery was observed in the mice that were given 100 mg/kg KRG The immunopositive staining of 8-oxoG was detected in the stria vascularis in the control group but was diminished in the mice that were given 200 mg/kg KRG The ingestion of more than 100 mg/kg KRG demonstrated a protection and recovery effect on the noiseinduced-TTS group. Since KRG has been reported to be a safe compound even up to hundreds of mg/kg, a higher concentration of it may effectively protect and recover TTS.

Ameliorating effect of the ethyl acetate fraction of Pteridium aquilinum on glucose-induced neuronal apoptosis (포도당으로 유도된 신경세포 손상에 대한 고사리 아세트산에틸 분획물의 개선 효과)

  • Park, Seon Kyeong;Guo, Tian Jiao;Kim, Jong Min;Kang, Jin Yong;Park, Sang Hyun;Kang, Jeong Eun;Kwon, Bong Seok;Lee, Chang Jun;Lee, Uk;Heo, Ho Jin
    • Korean Journal of Food Science and Technology
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    • v.49 no.4
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    • pp.430-437
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    • 2017
  • The protective effect of Pteridium aquilinum on high glucose-induced cytotoxicity was examined in vitro to investigate the relationship between diabetic condition and neuronal dysfunction. The ethyl acetate fraction of P. aquilinum (EFPA), with total phenolic content of 265.08 mg gallic acid equivalent/g, showed higher 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid)/2,2-diphenyl-1-picrylhydrazyl radical scavenging activities and lipid peroxidation inhibitory effect than any other fraction. In addition, EFPA showed a significant reduction in the inhibitory effect on ${\alpha}$-glucosidase activity ($IC_{50}$ value=$205.26{\mu}g/mL$) compared to the acarbose positive control. The anti-oxidative effect in PC12 cells, protective effects on high glucose-induced oxidative stress in neuronal cells, and neurotoxicity were measured using 2',7'-dichlorofluorescin diacetate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide, and lactate dehydrogenase assays, respectively. EFPA showed conspicuous inhibitory effect on cellular reactive oxygen species production and neuronal cell apoptosis. Finally, kaempferol-3-glucoside was identified as the main phenolic compound of EFPA using high performance liquid chromatography.