The Experts below are selected from a list of 2466 Experts worldwide ranked by ideXlab platform

Yang Chen - One of the best experts on this subject based on the ideXlab platform.

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Ping Xu, Mian Zhang, Ying Li, Yang Chen
    Abstract:

    Ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated NSAID-induced enteropathy in rats partly by inhibiting intestinal β-glucuronidase activity

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Mian Zhang, Binbin Sun, Nan Shu, Qiushi Xie, Yang Chen
    Abstract:

    Diclofenac is a non-steroidal anti-inflammatory drug (NSAID), which may cause serious intestinal adverse reactions (enteropathy). In this study we investigated whether co-administration of ciprofloxacin affected the pharmacokinetics of diclofenac and diclofenac-induced enteropathy in rats. The pharmacokinetics of diclofenac was assessed in rats after receiving diclofenac (10 mg/kg, ig, or 5 mg/kg, iv), with or without ciprofloxacin (20 mg/kg, ig) co-administered. After receiving 6 oral doses or 15 intravenous doses of diclofenac, the rats were sacrificed, and small intestine was removed to examine diclofenac-induced enteropathy. β-Glucuronidase activity in intestinal content, bovine liver and E coli was evaluated. Following oral or intravenous administration, the pharmacokinetic profile of diclofenac displayed typical Enterohepatic Circulation, and co-administration of ciprofloxacin abolished the Enterohepatic Circulation, resulted in significant reduction in the plasma content of diclofenac. In control rats, β-glucuronidase activity in small intestinal content was region-dependent: proximal intestinesmall intestine, and particularly in ileal valve. Furthermore, ciprofloxacin (10–2000 μmol/L) dose-dependently inhibited β-glucuronidase activity in distal small intestine content or E coli incubated in vitro, but did not affect that in proximal small intestine content or bovine liver incubated in vitro. After receiving 6 oral doses or 15 intravenous doses of diclofenac, typical enteropathy was developed with severe enteropathy occurred in distal small intestine. Co-administration of ciprofloxacin significantly alleviated diclofenac-induced enteropathy. Co-administration of ciprofloxacin attenuated Enterohepatic Circulation of diclofenac and alleviated diclofenac-induced enteropathy in rats, partly via the inhibition of intestinal β-glucuronidase activity.

Marilyn E. Morris - One of the best experts on this subject based on the ideXlab platform.

  • pharmacokinetics of the monocarboxylate transporter 1 inhibitor azd3965 in mice potential Enterohepatic Circulation and target mediated disposition
    Pharmaceutical Research, 2020
    Co-Authors: Xiaowen Guan, Marilyn E. Morris
    Abstract:

    To evaluate the pharmacokinetics (PK) of the monocarboxylate transporter 1 (MCT1) inhibitor AZD3965 in mice after IV and oral administration and to develop mechanistic PK models to assess the potential Enterohepatic Circulation (EHC) and target-mediated drug disposition (TMDD) of AZD3965. Female BALB/c mice were administered AZD3965 by IV injection (10, 50 and 100 mg/kg) or oral gavage (100 mg/kg). Plasma samples were analyzed using LC/MS/MS, and PK parameters determined by compartmental and non-compartmental analyses. AZD3965 exhibited a large volume of distribution and rapid oral absorption, with a high oral bioavailability. Prominent reentry peaks were observed after both oral and IV administration, suggesting potential EHC of AZD3965 or of a potential glucuronide conjugate. The dose-dependent studies indicated greater than proportional increases in exposure, an increase in the terminal half-life, and decrease in clearance and volume of distribution with increasing IV doses, indicating nonlinear pharmacokinetics and potential TMDD of AZD3965. Mechanistic compartmental models were developed to characterize the complex pharmacokinetics of AZD3965. The current study represents the first comprehensive report of the pharmacokinetics of AZD3965 in mice, indicating the potential contribution of EHC and TMDD in the disposition of AZD3965.

  • pharmacokinetics of the monocarboxylate transporter 1 inhibitor azd3965 in mice potential Enterohepatic Circulation and target mediated disposition
    Pharmaceutical Research, 2020
    Co-Authors: Xiaowen Guan, Marilyn E. Morris
    Abstract:

    To evaluate the pharmacokinetics (PK) of the monocarboxylate transporter 1 (MCT1) inhibitor AZD3965 in mice after IV and oral administration and to develop mechanistic PK models to assess the potential Enterohepatic Circulation (EHC) and target-mediated drug disposition (TMDD) of AZD3965. Female BALB/c mice were administered AZD3965 by IV injection (10, 50 and 100 mg/kg) or oral gavage (100 mg/kg). Plasma samples were analyzed using LC/MS/MS, and PK parameters determined by compartmental and non-compartmental analyses. AZD3965 exhibited a large volume of distribution and rapid oral absorption, with a high oral bioavailability. Prominent reentry peaks were observed after both oral and IV administration, suggesting potential EHC of AZD3965 or of a potential glucuronide conjugate. The dose-dependent studies indicated greater than proportional increases in exposure, an increase in the terminal half-life, and decrease in clearance and volume of distribution with increasing IV doses, indicating nonlinear pharmacokinetics and potential TMDD of AZD3965. Mechanistic compartmental models were developed to characterize the complex pharmacokinetics of AZD3965. The current study represents the first comprehensive report of the pharmacokinetics of AZD3965 in mice, indicating the potential contribution of EHC and TMDD in the disposition of AZD3965.

Zeyu Zhong - One of the best experts on this subject based on the ideXlab platform.

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Ping Xu, Mian Zhang, Ying Li, Yang Chen
    Abstract:

    Ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated NSAID-induced enteropathy in rats partly by inhibiting intestinal β-glucuronidase activity

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Mian Zhang, Binbin Sun, Nan Shu, Qiushi Xie, Yang Chen
    Abstract:

    Diclofenac is a non-steroidal anti-inflammatory drug (NSAID), which may cause serious intestinal adverse reactions (enteropathy). In this study we investigated whether co-administration of ciprofloxacin affected the pharmacokinetics of diclofenac and diclofenac-induced enteropathy in rats. The pharmacokinetics of diclofenac was assessed in rats after receiving diclofenac (10 mg/kg, ig, or 5 mg/kg, iv), with or without ciprofloxacin (20 mg/kg, ig) co-administered. After receiving 6 oral doses or 15 intravenous doses of diclofenac, the rats were sacrificed, and small intestine was removed to examine diclofenac-induced enteropathy. β-Glucuronidase activity in intestinal content, bovine liver and E coli was evaluated. Following oral or intravenous administration, the pharmacokinetic profile of diclofenac displayed typical Enterohepatic Circulation, and co-administration of ciprofloxacin abolished the Enterohepatic Circulation, resulted in significant reduction in the plasma content of diclofenac. In control rats, β-glucuronidase activity in small intestinal content was region-dependent: proximal intestinesmall intestine, and particularly in ileal valve. Furthermore, ciprofloxacin (10–2000 μmol/L) dose-dependently inhibited β-glucuronidase activity in distal small intestine content or E coli incubated in vitro, but did not affect that in proximal small intestine content or bovine liver incubated in vitro. After receiving 6 oral doses or 15 intravenous doses of diclofenac, typical enteropathy was developed with severe enteropathy occurred in distal small intestine. Co-administration of ciprofloxacin significantly alleviated diclofenac-induced enteropathy. Co-administration of ciprofloxacin attenuated Enterohepatic Circulation of diclofenac and alleviated diclofenac-induced enteropathy in rats, partly via the inhibition of intestinal β-glucuronidase activity.

Xiange Tang - One of the best experts on this subject based on the ideXlab platform.

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Ping Xu, Mian Zhang, Ying Li, Yang Chen
    Abstract:

    Ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated NSAID-induced enteropathy in rats partly by inhibiting intestinal β-glucuronidase activity

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Mian Zhang, Binbin Sun, Nan Shu, Qiushi Xie, Yang Chen
    Abstract:

    Diclofenac is a non-steroidal anti-inflammatory drug (NSAID), which may cause serious intestinal adverse reactions (enteropathy). In this study we investigated whether co-administration of ciprofloxacin affected the pharmacokinetics of diclofenac and diclofenac-induced enteropathy in rats. The pharmacokinetics of diclofenac was assessed in rats after receiving diclofenac (10 mg/kg, ig, or 5 mg/kg, iv), with or without ciprofloxacin (20 mg/kg, ig) co-administered. After receiving 6 oral doses or 15 intravenous doses of diclofenac, the rats were sacrificed, and small intestine was removed to examine diclofenac-induced enteropathy. β-Glucuronidase activity in intestinal content, bovine liver and E coli was evaluated. Following oral or intravenous administration, the pharmacokinetic profile of diclofenac displayed typical Enterohepatic Circulation, and co-administration of ciprofloxacin abolished the Enterohepatic Circulation, resulted in significant reduction in the plasma content of diclofenac. In control rats, β-glucuronidase activity in small intestinal content was region-dependent: proximal intestinesmall intestine, and particularly in ileal valve. Furthermore, ciprofloxacin (10–2000 μmol/L) dose-dependently inhibited β-glucuronidase activity in distal small intestine content or E coli incubated in vitro, but did not affect that in proximal small intestine content or bovine liver incubated in vitro. After receiving 6 oral doses or 15 intravenous doses of diclofenac, typical enteropathy was developed with severe enteropathy occurred in distal small intestine. Co-administration of ciprofloxacin significantly alleviated diclofenac-induced enteropathy. Co-administration of ciprofloxacin attenuated Enterohepatic Circulation of diclofenac and alleviated diclofenac-induced enteropathy in rats, partly via the inhibition of intestinal β-glucuronidase activity.

Zhaoli Ling - One of the best experts on this subject based on the ideXlab platform.

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Ping Xu, Mian Zhang, Ying Li, Yang Chen
    Abstract:

    Ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated NSAID-induced enteropathy in rats partly by inhibiting intestinal β-glucuronidase activity

  • ciprofloxacin blocked Enterohepatic Circulation of diclofenac and alleviated nsaid induced enteropathy in rats partly by inhibiting intestinal β glucuronidase activity
    Acta Pharmacologica Sinica, 2016
    Co-Authors: Zeyu Zhong, Xiange Tang, Zhaoli Ling, Fan Wang, Kaijing Zhao, Mian Zhang, Binbin Sun, Nan Shu, Qiushi Xie, Yang Chen
    Abstract:

    Diclofenac is a non-steroidal anti-inflammatory drug (NSAID), which may cause serious intestinal adverse reactions (enteropathy). In this study we investigated whether co-administration of ciprofloxacin affected the pharmacokinetics of diclofenac and diclofenac-induced enteropathy in rats. The pharmacokinetics of diclofenac was assessed in rats after receiving diclofenac (10 mg/kg, ig, or 5 mg/kg, iv), with or without ciprofloxacin (20 mg/kg, ig) co-administered. After receiving 6 oral doses or 15 intravenous doses of diclofenac, the rats were sacrificed, and small intestine was removed to examine diclofenac-induced enteropathy. β-Glucuronidase activity in intestinal content, bovine liver and E coli was evaluated. Following oral or intravenous administration, the pharmacokinetic profile of diclofenac displayed typical Enterohepatic Circulation, and co-administration of ciprofloxacin abolished the Enterohepatic Circulation, resulted in significant reduction in the plasma content of diclofenac. In control rats, β-glucuronidase activity in small intestinal content was region-dependent: proximal intestinesmall intestine, and particularly in ileal valve. Furthermore, ciprofloxacin (10–2000 μmol/L) dose-dependently inhibited β-glucuronidase activity in distal small intestine content or E coli incubated in vitro, but did not affect that in proximal small intestine content or bovine liver incubated in vitro. After receiving 6 oral doses or 15 intravenous doses of diclofenac, typical enteropathy was developed with severe enteropathy occurred in distal small intestine. Co-administration of ciprofloxacin significantly alleviated diclofenac-induced enteropathy. Co-administration of ciprofloxacin attenuated Enterohepatic Circulation of diclofenac and alleviated diclofenac-induced enteropathy in rats, partly via the inhibition of intestinal β-glucuronidase activity.