Stachydrine hydrochloride
Stachydrine hydrochloride promotes the protein expression of IL-12 and IL-6, as well as the mRNA expression of T-bet and RORγt, while inhibiting the mRNA expression of GATA-3 and Foxp3; the Th1/Th2/Th17/Treg paradigm induced by Stachydrine hydrochloride contributed to the reduction in uterine bleeding in RU486-induced abortion mice.
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Am J Transl Res . 2017 Apr 15;9(4):1834-1844. eCollection 2017.
Stachydrine hydrochloride inhibits proliferation and induces apoptosis of breast cancer cells via inhibition of Akt and ERK pathways[Pubmed:
28469788]
Abstract
Although a series of efficient Akt and ERK inhibitors have been developed to target breast cancer cells, drug resistance can emerge after long-term treatment. Therefore, it is essential to uncover alternative drugs for inhibiting survival pathways in breast cancer cells. Stachydrine hydrochloride, a well-known bioactive ingredients extracted from HerbaLeonuri, has proven to be very efficient for the treatment of various diseases such as prostate cancer. However, whether Stachydrine hydrochloride can exert similar prophylactic and therapeutic effects against breast cancer, and the probable underlying molecular mechanism remain unknown. In the present work, the effects of Stachydrine hydrochloride on human breast cancer cell lines (T47D and MCF-7) were evaluated. Our results showed that Stachydrine hydrochloride inhibits cell proliferation and induces primary apoptosis and ROS production in T47D and MCF-7 cells in time- and dose-dependent manner. Mechanistically, Stachydrine hydrochloride treatment induced caspase-3 activation and decreased the expression of the anti-apoptotic protein Bcl-2. Moreimportantly, Stachydrine hydrochloride simultaneously inhibited the phosphorylation of Akt and ERK proteins. Overall, our data indicated that Stachydrine hydrochloride induces apoptosis in MCF-7 and T47D cells and exerts inhibitory effects on proliferation by concurrently suppressing Akt and ERK survival signals, suggesting its potential efficiency in treatment of breast cancer.
Keywords: Akt; ERK; Stachydrine hydrochloride; apoptosis; breast cancer; proliferation.
J Ethnopharmacol. 2013 Jan 9;145(1):241-53.
The Th1/Th2/Th17/Treg paradigm induced by stachydrine hydrochloride reduces uterine bleeding in RU486-induced abortion mice.[Pubmed:
23178269]
Stachydrine hydrochloride is the main constituent of L. sibiricus, therefore L. sibiricus is regarded as a candidate for reducing uterine bleeding in RU486-induced abortion mice by regulating the Th1/Th2/Th17/Treg paradigm.
The purpose of this study was to determine the Th1/Th2/Th17/Treg paradigm in uterine bleeding of RU486-induced abortion mice and to elucidate the immunopharmacologic effects of Stachydrine hydrochloride on inducing the Th1/Th2/Th17/Treg paradigm in reducing the uterine bleeding volume in RU486-induced abortion mice.
METHODS AND RESULTS:
To investigate the Th1/Th2/Th17/Treg paradigm in uterine bleeding during RU486-induced abortion mice, pregnant BALB/c mice were treated with high- and low-dose RU486 (1.5mg/kg and 0.9 mg/kg, respectively), and the serum progesterone (P(4)) protein level, uterine bleeding volume, and proportions of Th1/Th2/Th17/Treg cells in mice at the maternal-fetal interface were detected by ELISA assay, alkaline hematin photometric assay, and flow cytometry, respectively. To determine the regulatory effect of Stachydrine hydrochloride on the Th1/Th2/Th17/Treg paradigm in vitro, splenocytes of non-pregnant mice were separated and treated with P(4,) RU486, and/or Stachydrine hydrochloride (10(-5)M, 10(-4)M, and 10(-3)M, respectively). The proportions of Th1/Th2/Th17/Treg cells were analyzed using flow cytometry. To evaluate the effect of Stachydrine hydrochloride in reducing uterine bleeding via regulation of the Th1/Th2/Th17/Treg paradigm, pregnant mice were treated with RU486 (1.5mg/kg) and/or Stachydrine hydrochloride (2.5mg/kg, 5mg/kg, and 10mg/kg). Stachydrine hydrochloride promoted the protein expression of IL-12 and IL-6, as well as the mRNA expression of T-bet and RORγt, while inhibiting the mRNA expression of GATA-3 and Foxp3. Therefore, the Th1/Th2/Th17/Treg paradigm in RU486-induced abortion mice shifted to Th1 and Th17 after Stachydrine hydrochloride administration. The volume of uterine bleeding during RU486-induced abortion was reduced significantly after Stachydrine hydrochloride administration.
CONCLUSIONS:
The Th1/Th2/Th17/Treg paradigm is closely related to the volume of uterine bleeding in RU486-induced abortion mice. The Th1/Th2/Th17/Treg paradigm induced by Stachydrine hydrochloride contributed to the reduction in uterine bleeding in RU486-induced abortion mice.
Am J Transl Res. 2017 Apr 15;9(4):1834-1844.
Stachydrine hydrochloride inhibits proliferation and induces apoptosis of breast cancer cells via inhibition of Akt and ERK pathways.[Pubmed:
28469788]
Although a series of efficient Akt and ERK inhibitors have been developed to target breast cancer cells, drug resistance can emerge after long-term treatment. Therefore, it is essential to uncover alternative drugs for inhibiting survival pathways in breast cancer cells. Stachydrine hydrochloride, a well-known bioactive ingredients extracted from HerbaLeonuri, has proven to be very efficient for the treatment of various diseases such as prostate cancer. However, whether Stachydrine hydrochloride can exert similar prophylactic and therapeutic effects against breast cancer, and the probable underlying molecular mechanism remain unknown.
METHODS AND RESULTS:
In the present work, the effects of Stachydrine hydrochloride on human breast cancer cell lines (T47D and MCF-7) were evaluated. Our results showed that Stachydrine hydrochloride inhibits cell proliferation and induces primary apoptosis and ROS production in T47D and MCF-7 cells in time- and dose-dependent manner. Mechanistically, Stachydrine hydrochloride treatment induced caspase-3 activation and decreased the expression of the anti-apoptotic protein Bcl-2. Moreimportantly, Stachydrine hydrochloride simultaneously inhibited the phosphorylation of Akt and ERK proteins.
CONCLUSIONS:
Overall, our data indicated that Stachydrine hydrochloride induces apoptosis in MCF-7 and T47D cells and exerts inhibitory effects on proliferation by concurrently suppressing Akt and ERK survival signals, suggesting its potential efficiency in treatment of breast cancer.
