Subchronic toxicity studies with ginsenoside compound K delivered to dogs via intravenous administration

2011 ◽  
Vol 49 (8) ◽  
pp. 1857-1862 ◽  
Author(s):  
Y.L. Gao ◽  
Z.F. Liu ◽  
C.M. Li ◽  
J.Y. Shen ◽  
H.X. Yin ◽  
...  
Keyword(s):  
Intravenous Administration ◽  
Compound K ◽  
Subchronic Toxicity ◽  
Toxicity Studies ◽  
Ginsenoside Compound K

Preclinical safety of ginsenoside compound K: Acute, and 26-week oral toxicity studies in mice and rats

2019 ◽  
Vol 131 ◽  
pp. 110578 ◽  
Author(s):  
Yonglin Gao ◽  
Tong Wang ◽  
Guangfei Wang ◽  
Guisheng Li ◽  
Chengfeng Sun ◽  
...  
Keyword(s):  
Compound K ◽  
Oral Toxicity ◽  
Toxicity Studies ◽  
Ginsenoside Compound K ◽  
Preclinical Safety

Acute and subchronic toxicity studies of rats exposed to vapors of methyl mercaptan and other reduced‐sulfur compounds

1981 ◽  
Vol 8 (1-2) ◽  
pp. 71-88 ◽  
Author(s):  
Martin F. Tansy ◽  
Frank M. Kendall ◽  
John Fantasia ◽  
Wendell E. Landin ◽  
Richard Oberly ◽  
...  
Keyword(s):  
Sulfur Compounds ◽  
Methyl Mercaptan ◽  
Reduced Sulfur Compounds ◽  
Subchronic Toxicity ◽  
Toxicity Studies ◽  
Reduced Sulfur

Subchronic Toxicity Studies of N-D-Ornithyl Amphotericin B Methyl Ester in Dogs and Rats

1985 ◽  
Vol 5 (4) ◽  
pp. 737-753
Author(s):  
TOBIAS MASSA ◽  
DINESH P. SINHA ◽  
JERRY D. FRANTZ ◽  
MARY E. FILIPEK ◽  
RAYMOND C. WEGLEIN ◽  
...  
Keyword(s):  
Methyl Ester ◽  
Amphotericin B ◽  
Subchronic Toxicity ◽  
Toxicity Studies ◽  
Amphotericin B Methyl Ester

scholarly journals Ginsenoside compound K induces apoptosis in nasopharyngeal carcinoma cells via activation of apoptosis-inducing factor

2014 ◽  
Vol 9 (1) ◽  
pp. 11 ◽  
Author(s):  
Carmen Ka-Man Law ◽  
Hoi-Hin Kwok ◽  
Po-Ying Poon ◽  
Chi-Chiu Lau ◽  
Zhi-Hong Jiang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Compound K ◽  
Ginsenoside Compound K ◽  
Apoptosis Inducing Factor

scholarly journals Production of bioactive ginsenoside compound K in metabolically engineered yeast

Cell Research ◽  
2014 ◽  
Vol 24 (6) ◽  
pp. 770-773 ◽  
Author(s):  
Xing Yan ◽  
Yun Fan ◽  
Wei Wei ◽  
Pingping Wang ◽  
Qunfang Liu ◽  
...  
Keyword(s):  
Compound K ◽  
Engineered Yeast ◽  
Ginsenoside Compound K

Ginsenoside compound K ameliorates Alzheimer’s disease in HT22 cells by adjusting energy metabolism

2019 ◽  
Vol 46 (5) ◽  
pp. 5323-5332 ◽  
Author(s):  
Xijun Chen ◽  
Hui Li ◽  
Qing Yang ◽  
Xingcheng Lan ◽  
Jifeng Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Energy Metabolism ◽  
Compound K ◽  
Ht22 Cells ◽  
Ginsenoside Compound K

scholarly journals Acute and Subchronic Toxicity Studies of Roots Barks Extracts of Calotropis procera (Ait.) R. Br Used in the Treatment of Sickle Cell Disease in Burkina Faso

2013 ◽  
Vol 4 (5) ◽  
pp. 194-200 ◽  
Author(s):  
Geoffroy G. Ouedraogo ◽  
Moustapha Ouedraogo ◽  
Assita Lamien-Sanou ◽  
Marius Lompo ◽  
Olga M. Goumbri-Lompo ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Burkina Faso ◽  
Sickle Cell ◽  
Calotropis Procera ◽  
Cell Disease ◽  
Subchronic Toxicity ◽  
Toxicity Studies

scholarly journals Ginsenoside Compound K Regulates HIF-1α-Mediated Glycolysis Through Bclaf1 to Inhibit the Proliferation of Human Liver Cancer Cells

2020 ◽  
Vol 11 ◽  
Author(s):  
Silin Zhang ◽  
Meilan Zhang ◽  
Jiaxin Chen ◽  
Jiaqi Zhao ◽  
Jielin Su ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Hepatoma Cells ◽  
Dependent Manner ◽  
Compound K ◽  
Liver Cancer Cells ◽  
Hypoxic Conditions ◽  
Huh7 Cells ◽  
Glycolysis Pathway ◽  
Ginsenoside Compound K

This study aimed to demonstrate that ginsenoside compound K (20 (S)-ginsenoside CK; CK) downregulates Bcl-2-associated transcription factor 1 (Bclaf1), which inhibits the hypoxia-inducible factor-1α (HIF-1α)-mediated glycolysis pathway to inhibit the proliferation of liver cancer cells. Treatment of hepatoma cells (Bel-7404 and Huh7) under hypoxic conditions with different concentrations of CK showed that CK inhibited the proliferation of hepatoma cells in a time- and concentration-dependent manner; furthermore, the ability of the cells to form colonies was reduced, and cell growth was blocked in the G0/G1 phase. CK promoted the degradation of HIF-1α ubiquitination in liver cancer cells by regulating the expression of HIF-1α and related ubiquitination proteins; moreover, it reduced the activity of key enzymes involved in glycolysis, the pressure of cellular glycolysis, and the rate of real-time ATP production, thereby inhibiting the glycolysis pathway. It also decreased the expression of Bclaf1 in hypoxic liver cancer cells and thus reduced the ability of Bclaf1 to bind to HIF-1α. CK treatment of Bel-7404 and Huh7 cells with CRISPR/Cas9-engineered knock out of Bclaf1 gene under hypoxic conditions further suppressed the expression of HIF-1α, promoted HIF-1α ubiquitination, and inhibited the glycolysis pathway. In a rat model of primary liver cancer induced by diethylnitrosamine, positron emission tomography and computed tomography scans showed that after CK administration, tumor tissue volumes were reduced and glucose uptake capacity decreased. Increased Bclaf1 and HIF-1α expression promoted the ubiquitination of HIF-1α and inhibited the glycolysis pathway, thereby inhibiting the proliferation of liver cancer cells. In summary, this study confirmed by in vitro and in vivo experiments that in hypoxic liver cancer cells CK downregulates the expression of Bclaf1, inhibits the HIF-1α-mediated glycolysis pathway, and inhibits cell proliferation, suggesting that the CK-mediated effects on Bclaf1 may represent a novel therapeutic approach for the treatment of liver cancer patients.

Genotoxicity and subchronic toxicity studies with heated olestra

1996 ◽  
Vol 34 (10) ◽  
pp. 941-950 ◽  
Author(s):  
G.M. Williams ◽  
M.J. Aardema ◽  
P.H. Long ◽  
E.D. Thompson ◽  
G.S. Allgood
Keyword(s):  
Subchronic Toxicity ◽  
Toxicity Studies
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