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

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Wei Peng, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

Mingjing Yi - One of the best experts on this subject based on the ideXlab platform.

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Wei Peng, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

Chun-su Yuan - One of the best experts on this subject based on the ideXlab platform.

  • Effect of Liquiritin on neuroendocrine‐immune network in menopausal rat model
    Phytotherapy research : PTR, 2020
    Co-Authors: Xin-yi Lan, Qiu-jing Chen, Shuo Zhai, Chun-feng Zhang, Chong-zhi Wang, Chun-su Yuan
    Abstract:

    Purpose The aim of the study was to investigate the effect of Liquiritin on neuroendocrine-immune network in menopausal rat model. Methods Liquiritin groups were respectively given Liquiritin suspension at the dose of 80, 40, and 20 mg/kg, once a day for continuous 30 days after the removal of bilateral ovaries to induce the menopausal rat model. Behavioral experiments were conducted and the organs were weighed for the viscera index. The content of estradiol (E2 ) and follicle-stimulating hormone (FSH) in the serum and 5-hydroxytryptamine (5-HT) and norepinephrine (NE) in hypothalamus were assayed by enzyme linked immunosorbent assay kits. Morphological changes of uterus and adrenal gland were observed by hematoxylin-eosin (HE) staining and estrogen receptor (ER) expression of uterus and spleen were determined by immunohistochemical staining. Results For the nervous system, Liquiritin relieved menopausal depression and up-regulated the levels of 5-HT and NE in hypothalamus; for the endocrine system, it raised the concentrations of E2 and FSH in serum, relieved the histological changes of uterus and adrenal gland and increased the expression of ER in uterus; for the immune system, it increased the thymus index and the expression of ER in spleen. Conclusions Liquiritin improved menopausal syndrome in multiple ways by affecting the neuro-endocrine-immune network.

  • effect of Liquiritin on neuroendocrine immune network in menopausal rat model
    Phytotherapy Research, 2020
    Co-Authors: Xin-yi Lan, Qiu-jing Chen, Shuo Zhai, Chun-feng Zhang, Chong-zhi Wang, Chun-su Yuan
    Abstract:

    Purpose The aim of the study was to investigate the effect of Liquiritin on neuroendocrine-immune network in menopausal rat model. Methods Liquiritin groups were respectively given Liquiritin suspension at the dose of 80, 40, and 20 mg/kg, once a day for continuous 30 days after the removal of bilateral ovaries to induce the menopausal rat model. Behavioral experiments were conducted and the organs were weighed for the viscera index. The content of estradiol (E2 ) and follicle-stimulating hormone (FSH) in the serum and 5-hydroxytryptamine (5-HT) and norepinephrine (NE) in hypothalamus were assayed by enzyme linked immunosorbent assay kits. Morphological changes of uterus and adrenal gland were observed by hematoxylin-eosin (HE) staining and estrogen receptor (ER) expression of uterus and spleen were determined by immunohistochemical staining. Results For the nervous system, Liquiritin relieved menopausal depression and up-regulated the levels of 5-HT and NE in hypothalamus; for the endocrine system, it raised the concentrations of E2 and FSH in serum, relieved the histological changes of uterus and adrenal gland and increased the expression of ER in uterus; for the immune system, it increased the thymus index and the expression of ER in spleen. Conclusions Liquiritin improved menopausal syndrome in multiple ways by affecting the neuro-endocrine-immune network.

Junjun Wang - One of the best experts on this subject based on the ideXlab platform.

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Wei Peng, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

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

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.

  • effect of hypaconitine combined with Liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo
    Journal of Pharmacy and Pharmacology, 2012
    Co-Authors: Mingjing Yi, Junjun Wang, Xiaomin Chen, Wei Peng, Yong Chen
    Abstract:

    OBJECTIVES: To study the effects of hypaconitine used alone and combined with Liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of Liquiritin on these hypaconitine-induced effects. METHODS: Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), Liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus Liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. KEY FINDINGS: The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with Liquiritin. Although CaM mRNA expression level was inhibited by Liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and Liquiritin significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. CONCLUSIONS: The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and Liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.