• Title/Summary/Keyword: phenol toxicity

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Hepatotoxicity and nephrotoxicity of saponin-enriched extract of Asparagus cochinchinensis in ICR mice

  • Sung, Ji Eun;Choi, Jun Young;Kim, Ji Eun;Lee, Hyun Ah;Yun, Woo Bin;Park, Jin Ju;Kim, Hye Ryeong;Song, Bo Ram;Kim, Dong Seob;Lee, Chung Yeoul;Lee, Hee Seob;Lim, Yong;Hwang, Dae Youn
    • Laboraroty Animal Research
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    • v.33 no.2
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    • pp.57-67
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    • 2017
  • The inhibitory effects of Asparagus cochinchinensis against inflammatory response induced by lipopolysaccharide (LPS), substance P and phthalic anhydride (PA) treatment were recently reported for some cell lines and animal models. To evaluate the hepatotoxicity and nephrotoxicity of A. cochinchinensis toward the livers and kidneys of ICR mice, alterations in related markers including body weight, organ weight, urine composition, liver pathology and kidney pathology were analyzed in male and female ICR mice after oral administration of 150, 300 and 600 mg/kg body weight/day saponin-enriched extract of A. cochinchinensis (SEAC) for 14 days. The saponin, total flavonoid and total phenol levels were found to be 57.2, 88.5 and 102.1 mg/g in SEAC, respectively, and the scavenging activity of SEAC gradually increased in a dose-dependent manner. Moreover, body and organ weight, clinical phenotypes, urine parameters and mice mortality did not differ between the vehicle and SEAC treated group. Furthermore, no significant alterations were measured in alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), blood urea nitrogen (BUN) and the serum creatinine (Cr) in the SEAC treated group relative to the vehicle treated group. Moreover, the specific pathological features induced by most toxic compounds were not observed upon liver and kidney histological analysis. Overall, the results of the present study suggest that SEAC does not induce any specific toxicity in the livers and kidneys of male and female ICR mice at doses of 600 mg/kg body weight/day.

Angiogenesis-inhibiting Effects of Prunus mume Butanol Fractions on Human Umbilical Vein Endothelial Cells (매실 부탄올 분획물에 의한 혈관 신생 억제 효과)

  • Min, Hye-Ji;Kim, Jeong-Ho;Heo, Ji-An;Won, Yeong-Seon;Seo, Kwon-Il
    • Journal of Life Science
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    • v.31 no.1
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    • pp.59-65
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    • 2021
  • Prunus mume Sieb. et Zucc is distributed throughout Asia and has traditionally been used as medicine and food. P. mume is known to contain large amounts of various organic acids, minerals, and phenol components. To date, the trend of P. mume research has focused only on the effects of antioxidant, anticancer and antibacterial, with only a few studies have focused on angiogenesis. Angiogenesis is a common characteristic of metastatic cancer through which oxygen and nutrients are delivered to the cells and tissues. In the present study, angiogenesis-inhibiting activity was investigated by evaluating the total polyphenol and flavonoid contents of the P. mume butanol fraction (PBF) and their ability to inhibit VEGF-induced human umbilical vein endothelial cells (HUVECs) proliferation, migration, invasion, and capillary formation. The polyphenols (12.81 mg GAE/g) and flavonoids (28.4 mg QE/g) of the PBF exhibited high antioxidant activity. The results of this study showed that PBF did not inhibit the proliferation of HUVECs at concentrations of 25-200 ㎍/ml and did not exhibit toxicity to normal cells. However, PBF inhibited the VEGF-induced mobility, invasion, and capillary formation of HUVECs. These results show that PBF inhibits the angiogenesis of HUVECs induced by VEGF. Therefore, PBF could serve as a therapeutic agent for the inhibition of angiogenesis.

Inhibitory Effects of Asparagus cochinchinensis in LPS-Stimulated BV-2 Microglial Cells through Regulation of Neuroinflammatory Mediators, the MAP Kinase Pathway, and the Cell Cycle (Lipopolysaccharide로 자극된 BV-2 미세교세포에서 신경염증 매개체, MAP kinase경로, 세포주기의 조절에 의한 천문동(Asparagus cochinchinensis)의 저해효과)

  • Lee, Hyun Ah;Kim, Ji Eun;Choi, Jun Young;Sung, Ji Eun;Youn, Woo Bin;Son, Hong Joo;Lee, Hee Seob;Kang, Hyun-Gu;Hwang, Dae Youn
    • Journal of Life Science
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    • v.30 no.4
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    • pp.331-342
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    • 2020
  • The suppression of neuroinflammatory responses in microglial cells can be considered a key target for improving the progression of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Asparagus cochinchinensis has traditionally been used as a medicine to treat fever, cough, kidney disease, breast cancer, inflammatory diseases, and brain diseases. In this study, we investigated the neuroprotective mechanism of an aqueous extract from A. cochinchinensis root (AEAC), particularly its anti-inflammatory effects on lipopolysaccharide (LPS)-activated BV-2 microglial cells. BV-2 cells were treated with four different concentrations of AEAC. No significant toxicity was detected in BV-2 cells treated with AEAC. Nitric oxide (NO), cyclooxygenase-2 (COX-2) mRNA, and inducible nitric oxide synthase (iNOS) mRNA levels were 21% lower in the AEAC+LPS group than in the Vehicle+LPS group. Lower proinflammatory (TNF-α and IL-1β) and anti-inflammatory cytokine (IL-6 and IL-10) levels were also detected in the AEAC+LPS group than in the Vehicle+LPS group, albeit at varying rates. Moreover, the phosphorylation of mitogen-activated protein kinase (MAPK) members after LPS treatment was significantly recovered in the AEAC-pretreated group compared to the Vehicle+LPS group, enhancement of the phosphorylation of mitogen-activated protein kinase (MAPK) members after LPS treatment was significantly recovered in the AEAC-pretreated group, while cell cycle arrest at the G2/M phase caused by LPS treatment was less severe in the AEAC+LPS group. The increase in reactive oxygen species (ROS) generation induced by LPS treatment was also lower in the AEAC-pretreated group than in the Vehicle+LPS group. This is the first study to show that AEAC exerts anti-neuroinflammatory activity against LPS stimulation by regulating the MAPK signaling pathway, the cell cycle, and ROS production.