Human PXR-mediated transcriptional activation of CYP3A4 by ‘Fuzi’ extracts

Huang, Guang-yao; Yang, Liang; Zhang, Zhaoyan; Ren, Shi‐Bin; Tang, Xiao‐Qing; Zhou, Wei; Wang, Yuguang; Gao, Shan; Gao, Yue

doi:10.1080/15376516.2018.1534296

Cited by 6 publications

(3 citation statements)

References 41 publications

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“…In another study, our team explored the components of FZ water and ethanol extracts. Moreover, the DDAs were quantified [ 42 ]. The differences in the metabolism of small molecules between the control group and the rats given FZ extracts showed that the extracts affected the metabolism, with different effects on the organs.…”

Section: Discussionmentioning

confidence: 99%

Study on Cardiotoxicity and Mechanism of “Fuzi” Extracts Based on Metabonomics

Huang

Yang

Zhou

et al. 2018

IJMS

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To investigate the toxicity of water and ethanol “Fuzi” (FZ) extracts and to explore the toxicity mechanism in rats. Water and ethanol extracts were prepared. Three groups of rats received the water extract, ethanol extract, or water by oral gavage for seven days. Pathological section staining of heart tissue. Colorimetric analysis was used to determine serum lactate dehydrogenase. The metabolic expression of small molecules in rats was measured by a metabolomics method. Western blotting was used to detect the expression of phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), transforming growth factor-β1 (TGF-β1), and caspase-3. Immunohistochemistry was used to detect the expression of CTnI, mTOR, and TGF-β1. The water and ethanol FZ extracts exert cardiotoxic effects via activating the PI3K/Akt/mTOR signaling pathway to induce cardiomyocyte apoptosis.

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Section: Discussionmentioning

confidence: 99%

Study on Cardiotoxicity and Mechanism of “Fuzi” Extracts Based on Metabonomics

Huang

Yang

Zhou

et al. 2018

IJMS

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“…As the key toxic and effective components in Aconiti Lateralis Radix, the concentration of DAs is strictly controlled [41]. Pharmacokinetic changes for DAs when there is combined utilization of P. ginseng may lead to a double-sided result.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Evaluation of the Influence of Panax ginseng on the Pharmacokinetics of Three Diester Alkaloids after Oral Administration of Aconiti Lateralis Radix in Rats Using UHPLC/QQQ‐MS/MS

Yang

Wang

Huang

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Objectives To investigate whether Panax ginseng (P. ginseng) could affect the metabolism of Diester Alkaloids (DAs) derived from Aconiti Lateralis Radix in vivo. Methods and Results 24 male Sprague-Dawley rats were randomized for 7-day treatment with P. ginseng (low, middle, and high), or vehicle. Aconiti Lateralis Radix was administered orally to each group on the 8th day. Plasma samples were collected, and Xevo TQ-S was used to detect the concentration of aconitine, mesaconitine, and hypaconitine in plasma. We describe a fast and reproducible method to detect the concentration of aconitine, mesaconitine, and hypaconitine in plasma. Compared to the control group, the AUC(0-t) of three DAs increased in both the middle and high dosing groups. The Vz/F of three DAs in these groups as well as the CLz/F of aconitine in all P. ginseng groups and the CLz/F of mesaconitine and hypaconitine in P. ginseng middle and high groups were decreased compared to the control group. Conclusion Orally administrated P. ginseng potentially inhibits the metabolism of DAs from Aconiti Lateralis Radix in rats.

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“…22 Cytochrome P450 (CYP) is a superfamily of enzymes which can be linked by exogenous compounds and metabolism of endogenous, including steroids, a number of medicines, fatty acids, and a number of chemicals P450 cytochrome is a superfamily of enzymes which can be linked by exogenous compounds and endogenous metabolism, including steroids, a number of medicines, fatty acids, and a number of smaller chemical molecules. 23 Cytochrome P450 CYP2E1, which has a large influence on oxidative stress, metabolic transformation, and other reactions, is one of the major metabolistic enzymes in the liver. In addition, the metabolic excitation of toxins is mainly mediated by CYP2E1.…”

Section: Introductionmentioning

confidence: 99%

Triptolide regulates oxidative stress and inflammation leading to hepatotoxicity via inducing CYP2E1

et al. 2021

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Triptolide (TP), the main active compound extracted from medicine— tripterygium wilfordii Hook f. (TWHF). It has anti-tumor and immunomodulatory properties. Our study aimed to investigate the mechanisms of hepatotoxicity treated with TP in vivo and in vitro, as well as their relationship with the NF-κB (p65) signal pathway; and to assess TP-induced hepatotoxicity after CYP2E1 modulation by the known inhibitor, clomethiazole, and the known inducer, pyrazole. Mice were given TP to cause liver injury and IHHA-1 cells were given TP to cause hepatocyte injury. The enzyme activity and hepatotoxicity changed dramatically when the CYP2E1 inhibitor and inducer were added. In comparison to the control group, the enzyme inducer increased the activity of CYP2E1, whereas the enzyme inhibitor had the opposite effect. Our findings suggest that TP is an inducer of CYP2E1 via a time-dependent activation mechanism. In addition, TP can promote oxidative stress, inflammatory and involving the NF-κB (p65) signal pathway. Therefore, we used triptolide to stimulate C57 mice and IHHA-1 cells to determine whether TP can promote oxidative stress and inflammation by activating CYP2E1 in response to exacerbated liver damage and participate in NF-κB (p65) signaling pathway.

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Human PXR-mediated transcriptional activation of CYP3A4 by ‘Fuzi’ extracts

Cited by 6 publications

References 41 publications

Study on Cardiotoxicity and Mechanism of “Fuzi” Extracts Based on Metabonomics

Study on Cardiotoxicity and Mechanism of “Fuzi” Extracts Based on Metabonomics

Simultaneous Evaluation of the Influence of Panax ginseng on the Pharmacokinetics of Three Diester Alkaloids after Oral Administration of Aconiti Lateralis Radix in Rats Using UHPLC/QQQ‐MS/MS

Triptolide regulates oxidative stress and inflammation leading to hepatotoxicity via inducing CYP2E1

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