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Fluorescence in Phytopreparations
Published in Victoria Vladimirovna Roshchina, Fluorescence of Living Plant Cells for Phytomedicine Preparations, 2020
Victoria Vladimirovna Roshchina
The complex phytopreparation Papilite is based on the oil from Chelidonium majus that includes more than 40 other medicinal valuable components, such as propolis (a waxy glue made by bees), Melaleuca alternifolia, mimeo or shilajt, brakshun, oleum Hippophae, castorium of beaver, etc. This preparation has been applied to papillomas with visible success. Effective application occurs due to alkaloids such as chelerythrine, sanguinarine, and others. In Figure 5.2, besides maximum of chlorophyll peak 675–680 nm, one can see in the fluorescence spectra the characteristic maximum in the 540–600 nm range, which includes the contribution mainly of the above-mentioned alkaloids. In any case, the emission with a peak 575 nm of the main active drug alkaloid, chelerythrine, of Chelidonium majus (Golovkin et al. 2001), is predominant in the probe and show antifungal features (Parvu et al. 2013).
Catalog of Herbs
Published in James A. Duke, Handbook of Medicinal Herbs, 2018
Numerous alkaloids have been reported from the celandine: allocryptopine, berberine, cheladimine, chelamine, chelerythrine, chelidamine, chelidonine, chelilutine, chelirubine, choline, coptisine, corysamine, dihydrosanguinarine, homochelidonine, hydroxychelidon-ine, hydroxysanguinanine, methoxychelidonine, oxychelidonine, oxysanguinarine, proto-pine, sanguinarine, sparteine, stylopine, and tetrahydrocoptisine.91 Since chelerythrine is described as “narcotic” by Grieve (meaning poisonous), there has been quite an interest in celandine in the counterculture. Sanguinarine stimulates intestinal paralysis and salivary secretions.16
Inhibiting Low-Density Lipoproteins Intimal Deposition and Preserving Nitric Oxide Function in the Vascular System
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Chelerythrine isolated from the wood of Toddalia asiatica (L.) Lam at a concentration of 100 μg/mL inhibited by 100% platelet aggregation induced by ADP, arachidonic acid, collagen and platelet activating factor.209 From the same plant, 2,6-dimethoxy-p-benzoquinone (Figure 5.19) at a concentration of 100 μg/mL inhibited by 100% platelet aggregation induced by arachidonic acid, collagen and platelet activating factor.209 Isopimpinellin at a concentration of 50 μg/mL inhibited the aggregation of platelets challenged with arachidonic acid.209 Chelerythrine a concentration of 25 μg/mL abrogated the aggregation of platelets induced by thrombin.209
Sanguinarine inhibits melanoma invasion and migration by targeting the FAK/PI3K/AKT/mTOR signalling pathway
Published in Pharmaceutical Biology, 2023
Xiaoyi Qi, Yonglan Chen, Sha Liu, Li Liu, Zehui Yu, Ling Yin, Lu Fu, Mingming Deng, Sicheng Liang, Muhan Lü
In addition to the FAK-PI3K-AKT-mTOR signalling pathway, SAG is reported to be against melanoma through other molecular signalling pathways, suggesting the concerted contribution to the action of SAG. Interestingly, it has been reported that structural analogues of SAG from Macleaya cordata, including chelerythrine, chelidonine, and chelilutine have potent anticancer activities. For example, chelerythrine inhibits the metastasis of hepatocellular carcinoma via PI3K/Akt/mTOR (Zhu et al. 2018); chelidonine inhibits the growth of gefitinib-resistant non-small cell lung cancer cells via the EGFR-AMPK pathway (Xie et al. 2020); chelilutine induces apoptosis by reducing the levels of anti-apoptotic proteins (Bcl-xL, Mcl-1, XIAP) (Slunská et al. 2010). This suggests that different alkaloids in Macleaya cordata might contribute to the overall anticancer effect via multiple molecular mechanisms.
Dexmedetomidine modulates mitochondrial dynamics to protect against endotoxin-induced lung injury via the protein kinase C-ɑ/haem oxygenase-1 signalling pathway
Published in Biomarkers, 2022
Kai Song, Jia Shi, Lina Zhan, Qiaoying Gao, Jing Yang, Shuan Dong, Yuan Zhang, Jianbo Yu
Mice in L group were injected intraperitoneally with LPS (10 mg/kg, dissolved in 0.9% saline) to establish a model of endotoxin-induced ALI (MacGarvey et al. 2012, Wang et al. 2018). In treatment groups (LDA1 and LDA2 groups), mice were injected intraperitoneally with DEX (70 μg/kg or 20 μg/kg, dissolved in 0.9% saline) (Fu et al. 2017, Zhang et al.2017, Li et al. 2018, Zhao et al. 2018, Xue et al. 2019, Chen et al.2020) once daily for three consecutive days before model preparation. Mice in the LDP group were injected intraperitoneally with DEX (70 µg/kg) followed 1 h later by 6 mg/kg of the PKC inhibitor, CHE (Mehrdad et al. 2020) (6 mg/kg, dissolved in 0.9% saline), for all three days. Mice in the LDP group were injected intraperitoneally with 10 mg/kg LPS (2 mg/mL, dissolved in 0.9% saline) (Wepler et al. 2019) 1 h after the last injection of CHE. The control group was injected with an equal volume of normal saline and CHE group was only injected with chelerythrine (6 mg/kg) intraperitoneally for three days. Twelve hours after LPS injection, the mice were euthanized, and lung tissue specimens were removed for analyses. The left lung was used for pathological observation. The weights of the lung tissue of the superior lobe of the right lung were used to determine the wet-to-dry (W/D) weight ratio before and after constant drying at 80 °C for 48 h, and the left lung was used for tissue gene and protein detection.
NURR1 inhibition reduces hypoxia-mediated cardiomyocyte necrosis via blocking Mst1-JNK-mPTP pathway
Published in Journal of Receptors and Signal Transduction, 2019
Ultimately, we want to explore whether Mst1-JNK pathway is required for mPTP opening regulation induced by hypoxia [61]. To address this question, an agonist of Mst1, chelerythrine, was added into the medium of cardiomyocyte treated with NURR1 siRNA [62]. As shown in Figure 5(A), compared to the control group, hypoxia-induced mPTP opening could be reversed by NURR1 deletion. Interestingly, chelerythrine treatment could re-caused mPTP opening although cardiomyocyte transfected with NURR1 siRNA. Therefore, this information indicated that NURR1 modulated mPTP opening via the Mst1-JNK pathway. Besides, the transcription of VDAC and CypD were also increased after exposure to hypoxia treatment and were reduced by NURR1 deletion (Figure 5(B,C)). However, chelerythrine treatment could abolish NURR1 deletion-mediated VDAC and CypD downregulation. This information further demonstrated the necessary role played by Mst1-JNK pathway in regulating mPTP opening in cardiomyocyte under hypoxia.