Efficacy, chemical composition, and pharmacological effects of herbal drugs derived from Fritillaria cirrhosa D. Don and Fritillaria thunbergii Miq.

Fritillaria cirrhosa D. Don and F. thunbergii Miq. belong to the genus Fritillaria within the Liliaceae family. They are used in traditional Chinese medicines that are often administered in clinical settings as they have notable effects on cough, bronchitis, pneumonia, lung injury, cancer, and other diseases. In this review, we focus on the history, origin, similarities, and differences in efficacy, chemical composition, and pharmacological outcomes of the drugs obtained from F. cirrhosa (FRC) and F. thunbergii (FRT). We list various valuable pharmacological effects of FRC and FRT, including antitussive, expectorant, anti-inflammatory, antioxidant, and anticancer effects. Thus, this review offers a basis for the medical application of and further research into the pharmacological impacts of these two drugs. We believe that new drugs derived from the phytoconstituents of F. cirrhosa and F. thunbergii that have specific therapeutic properties can be developed in the future.

Maternal vitamin D supplementation inhibits bisphenol A-induced proliferation of Th17 cells in adult offspring.

Bisphenol A (BPA) exposure can increase the risk of immune-related diseases in later life. Vitamin D3 (Vit D3) has been shown to have multiple immunomodulatory actions and has been used to treat immune diseases. However, the potential beneficial effects of Vit D3 on BPA-induced adverse effects in the immune system have not explored. We hypothesize that VitD3 may ameliorate BPA-induced side effects in the immune system, even in offspring of VitD3-supplemented mothers. Here, we established our experimental model by exposing pregnant dams with 1000 nM BPA with or without VitD3 (0.25 µg/kg, 1 µg/kg and 4 µg/kg) treatment. We show that mother's exposure to BPA increases proliferation of the spleen T helper 17 (Th17) cells and serum protein level of IL-17 in the offspring; however, VitD3 supplementation in mothers dose-dependently ameliorated these BPA-induced side effects on the immune system in the offspring as evidenced by attenuated upregulation of Th17 proliferation, and RORγt, IL-17, IL-6, and IL-23 expressions in the offspring. Our data provide the first evidence that maternal VitD3 supplementation offers benefits to the offspring by attenuating BPA-induced side effects on the immune system through vitamin D receptor (VDR)-dependent regulation of transcription factors and cytokines, suggesting its translational potential.

Inhibition of acquired-resistance hepatocellular carcinoma cell growth by combining sorafenib with phosphoinositide 3-kinase and rat sarcoma inhibitor.

BACKGROUND: To provide support for combined usage of phosphoinositide 3-kinase (PI3K) inhibitors or mitogen-activated protein kinase pathway inhibitors together with sorafenib in treatment of sorafenib-resistant hepatocellular carcinoma. MATERIALS AND METHODS: The sorafenib-resistant cell lines were established to evaluate the effects of MK-2206 2HCL, a dual PI3K/mammalian target of rapamycin (mTOR) inhibitor, and PD0325901, an rat sarcoma (RAS) and/or extracellular signal-regulated kinase (ERK) inhibitor, on cell proliferation and apoptosis, as both single and combined treatments with sorafenib. In addition, multidrug resistance 1 gene expression, mutation status of key members in PI3K/mTOR, and RAS/ERK pathways and pathway activation were analyzed to identify predictors of drug response. RESULTS: Molecular studies reveal that combining MK-2206 2HCL or PD0325901 with sorafenib not only has a synergistic effect, in suppressing PI3K/protein kinase B/mTOR and RAS/MEK/ERK signaling more effectively than either treatment alone, but also prevents the cross activation of the other pathway that occurs with single treatments in both sorafenib sensitive and resistant lines. PD0325901 exhibited a stronger synergic effect with sorafenib than MK-2206 2HCL. Sorafenib-resistant cell lines were characterized by activation of both of the two pathways, as indicated by multidrug resistance 1 gene expression profiles and pathway activity analysis. CONCLUSIONS: Our studies have showed that both inhibitors of PI3K/mTOR and RAS/ERK signaling are potentially effective antihepatocellular carcinoma drugs especially in treating sorafenib-resistant hepatocellular carcinoma.