1.Research advances in hepatic fibrosis related signal pathways and anti-hepatic fibrosis drugs
Suriguga LU ; Ting LIU ; Dandan ZHU ; Sijia YU ; Liqing LU ; Junjie DING
Journal of Clinical Hepatology 2022;38(5):1161-1164
Hepatic fibrosis is a pathological process in which the liver is subjected to various acute and chronic injuries for a long time, resulting in activation of hepatic stellate cells, the imbalance between the production and degradation of extracellular matrix, and the deposition of extracellular matrix in the liver, and it is jointly controlled by multiple cellular signal transduction pathways and a series of cellular information molecular networks. If there is no effective treatment, with the progression of the disease, liver fibrous nodules will form, destroy normal liver structure and function, and finally develop into liver cirrhosis, the decline of liver function, and even liver cancer. This article summarizes the research advances in the signaling pathways, receptors, and non-coding RNAs involved in liver fibrosis and the corresponding anti-hepatic fibrosis drugs/molecules.
2.HPLC analysis of 16 compounds from Artemisia ordosica.
Xiurong KANG ; Qinghu WANG ; Suriguga AO ; MOXIYELE ; Wenlin BAO ; Chaoliang ZHAO
Chinese Herbal Medicines 2023;15(2):337-342
OBJECTIVE:
To establish a high-performance liquid chromatographic method (HPLC) for the simultaneous determination of 16 compounds from Artemisia ordosica.
METHODS:
HPLC was used to analyze 16 quality indicators of A. ordosica. The HPLC conditions were as follows: Agilent Eclipse Plus C18 column (250 mm × 4.6 mm, 5 μm) with acetonitrile (A)-water (B) as mobile phase, gradient elution: 0-10 min, 75%-65% B; 10-30 min, 65%-35% B; and finally 30-40 min, 35%-15% B. The flow rate was 1.0 mL/min, the column temperature was 40 °C, the injection volume was 10 μL, and monitored by absorbance at 285 nm for compounds 1- 10, 12 and 225 nm for compounds 11, 13- 16.
RESULTS:
Under the selected experimental chromatographic conditions, compounds 1- 16 showed good linearity (r > 0.9993) in a wide concentration range. Their average recoveries were 99.50%, 95.38%, 97.75%, 96.00%, 98.20%, 97.50%, 95.50%, 99.33%, 96.75%, 96.50%, 98.50%, 97.83%, 99.20%, 95.33%, 97.33% and 96.30%, respectively, and the RSD were 1.99%, 1.81%, 1.63%, 1.98%, 1.67%, 1.92%, 1.74%, 1.67%, 1.90%, 1.72%, 1.88%, 1.83%, 1.79%, 1.76%, 1.81% and 1.96%, respectively.
CONCLUSION
Based on the results of the HPLC analysis, it was concluded that p-hydroxycinnamic acid ( 1), O-hydroxycinnamic acid ( 2), coniferyl alcohol ( 5), 5,4'-dihydroxy-7,3'-dimethoxyflavanone ( 8), 5,4'-dihydroxy-7-methoxyflavanone ( 9), 5-hydroxy-7,4'-dimethoxyflavanone ( 12), dehydrofalcarindiol ( 13), arteordoyn A ( 14), dehydrofalcarinol ( 15) and capillarin ( 16) are best suited for the role of quality indicators of A. ordosica grown in different ecological environments.
3.The role of ROS in hydroquinone-induced inhibition of K562 cell erythroid differentiation.
Chun Hong YU ; Suriguga ; Yang LI ; Yi Ran LI ; Ke Ya TANG ; Liang JIANG ; Zong Chun YI
Biomedical and Environmental Sciences 2014;27(3):212-214
The role of ROS in hydroquinone-induced inhibition of K562 cell erythroid differentiation was investigated. After K562 cells were treated with hydroquinone for 24 h, and hemin was later added to induce erythroid differentiation for 48 h, hydroquinone inhibited hemin-induced hemoglobin synthesis and mRNA expression of γ-globin in K562 cells in a concentration-dependent manner. The 24-h exposure to hydroquinone also caused a concentration-dependent increase at an intracellular ROS level, while the presence of N- acetyl-L-cysteine prevented hydroquinone- induced ROS production in K562 cells. The presence of N-acetyl-L-cysteine also prevented hydroquinone inhibiting hemin-induced hemoglobin synthesis and mRNA expression of γ-globin in K562 cells. These evidences indicated that ROS production played a role in hydroquinone-induced inhibition of erythroid differentiation.
Acetylcysteine
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pharmacology
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Cell Differentiation
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drug effects
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Dose-Response Relationship, Drug
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Hemin
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pharmacology
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Humans
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Hydroquinones
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pharmacology
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K562 Cells
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drug effects
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Reactive Oxygen Species
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metabolism
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gamma-Globins
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genetics