Cyanidin Chloride is a subclass of anthocyanidins possessing antioxidant and anticancer activities[1-2]. Cyanidin Chloride can inhibit RANKL-induced NF-κB activation, IκB-α degradation, and ERK phosphorylation to reduce bone resorption. Cyanidin Chloride can be used for research related to osteoporosis and cancer[3-4].
In vitro, MC3T3-E1 cells were treated with Cyanidin Chloride (5mg/mL) for 24 hours. Cyanidin Chloride significantly reversed the decreased cell viability and increased apoptosis level caused by XIST overexpression. Cyanidin Chloride simultaneously enhanced intracellular alkaline phosphatase (ALP) activity and the expression of bone morphogenetic protein 2 (BMP2) and osteocalcin (OCN)[5]. Human colorectal cancer HCT116, HT29, and SW620 cells were treated with Cyanidin Chloride (50–100μM) for 24 hours. Under TNF-α stimulation, Cyanidin Chloride significantly inhibited cell proliferation and induced apoptosis. Cyanidin Chloride suppressed the NF-κB signaling pathway by inhibiting the phosphorylation of IκBα and IKKα/β and blocking the nuclear translocation of p65/p50. Cyanidin Chloride activated the Nrf2 antioxidant pathway by promoting Nrf2 nuclear translocation and binding to the ARE promoter[6].
In vivo, C57BL/6J mice with acute or chronic cardiomyopathy were treated with Cyanidin Chloride (Acute model: 100 or 200mg/kg/day; intragastrically administered; for 8 days. Chronic model: 50mg/kg/day; intragastrically administered; for 5 weeks). Cyanidin Chloride significantly ameliorated the Doxorubicin-induced decline in cardiac function. Cyanidin Chloride reduced inflammatory cell infiltration, iron deposition, and the level of the lipid peroxidation metabolite MDA in heart tissue. Cyanidin Chloride also reversed ultrastructural mitochondrial damage and the downregulated expression of proteins including Nrf2, Gpx4, and PGC1 in the heart[7]. C57BL/6J mice intranasally infected with the MRSA USA300 strain were subcutaneously administered Cyanidin Chloride (80mg/kg). Administration began 1 hour post-infection and was repeated every 12 hours for 4 days. Cyanidin Chloride significantly increased the survival rate of infected mice. Cyanidin Chloride also significantly reduced the bacterial load in lung tissue and alleviated pulmonary congestion and inflammatory cell infiltration[8].
References:
[1] Qu D, Ye Z, Zhang W, et al. Cyanidin Chloride Improves LPS-Induced Depression-Like Behavior in Mice by Ameliorating Hippocampal Inflammation and Excitotoxicity. ACS Chem Neurosci. 2022 Nov 2;13(21):3023-3033.
[2] Cheng J, Zhou L, Liu Q, et al. Cyanidin Chloride inhibits ovariectomy-induced osteoporosis by suppressing RANKL-mediated osteoclastogenesis and associated signaling pathways. J Cell Physiol. 2018 Mar;233(3):2502-2512.
[3] Jiang L, Li Z, Xie Y, et al. Cyanidin chloride modestly protects Caco-2 cells from ZnO nanoparticle exposure probably through the induction of autophagy. Food Chem Toxicol. 2019 May;127:251-259.
[4] Takahama U, Hirota S, Yanase E. Slow starch digestion in the rice cooked with adzuki bean: Contribution of procyanidins and the oxidation products. Food Res Int. 2019 May;119:187-195.
[5] Zhang Y, Yuan Q, Wei Q, et al. Long noncoding RNA XIST modulates microRNA-135/CREB1 axis to influence osteogenic differentiation of osteoblast-like cells in mice with tibial fracture healing. Hum Cell. 2022 Jan;35(1):133-149.
[6] Lee DY, Yun SM, Song MY, et al. Cyanidin Chloride Induces Apoptosis by Inhibiting NF-κB Signaling through Activation of Nrf2 in Colorectal Cancer Cells. Antioxidants (Basel). 2020 Mar 27;9(4):285.
[7] Liu C, Wang Y, Zeng Y, et al. Use of Deep-Learning Assisted Assessment of Cardiac Parameters in Zebrafish to Discover Cyanidin Chloride as a Novel Keap1 Inhibitor Against Doxorubicin-Induced Cardiotoxicity. Adv Sci (Weinh). 2023 Oct;10(30):e2301136.
[8] Su X, Yu H, Wang X, et al. Cyanidin chloride protects mice from methicillin-resistant Staphylococcus aureus-induced pneumonia by targeting Sortase A. Virulence. 2022 Dec;13(1):1434-1445.
Cyanidin Chloride是一种花青素的亚类，具有抗氧化和抗癌活性[1-2]。Cyanidin Chloride可抑制RANKL诱导的NF-κB激活、IκB-α降解和ERK磷酸化以减少骨吸收。Cyanidin Chloride可用于骨质疏松症和癌症的相关研究[3-4]。
在体外，Cyanidin Chloride（5mg/mL）处理MC3T3-E1细胞24小时。Cyanidin Chloride能够显著逆转因XIST过表达导致的细胞活力下降和凋亡水平升高，同时增强细胞内的碱性磷酸酶（ALP）活性以及骨形态发生蛋白2（BMP2）和骨钙素（OCN）的表达[5]。Cyanidin Chloride（50–100μM）处理人结肠癌HCT116、HT29和SW620细胞24小时。在TNF-α刺激下，Cyanidin Chloride可显著抑制细胞增殖并诱导细胞凋亡，同时通过抑制IκBα和IKKα/β的磷酸化、阻断p65/p50核转位来抑制NF-κB信号通路，并通过促进Nrf2核转位和与ARE启动子结合来激活Nrf2抗氧化通路[6]。
在体内，Cyanidin Chloride（急性模型：100或200mg/kg/day；灌胃给药；连续8天；慢性模型：50mg/kg/day；灌胃给药；连续5周）用于处理急性或慢性心肌病C57BL/6J小鼠。Cyanidin Chloride显著改善了因阿霉素导致的心脏功能下降，减少了心脏组织中的炎症细胞浸润、铁沉积和脂质过氧化代谢物MDA水平，并逆转了心脏中线粒体结构损伤以及Nrf2、Gpx4、PGC1等蛋白的表达下调[7]。Cyanidin Chloride（80mg/kg）皮下注射于经鼻感染MRSA USA300菌株的C57BL/6J小鼠，在感染后1小时开始给药，之后每12小时一次，连续4天。Cyanidin Chloride显著提高感染小鼠的存活率，同时显著降低了肺组织中的细菌负荷，并减轻了肺组织的充血和炎症细胞浸润[8]。