Callistephin (chloride)

Callistephin (Pelargonidin 3-O-glucoside) chloride is an anthocyanin. Callistephin chloride regulates the expression of inflammatory (reducing iNOS/TNF-α/COX-2) and apoptosis-related proteins by inhibiting p38 phosphorylation, and enhances the protective effect of Isoflurane (HY-A0134) on microglial cell damage. Callistephin chloride significantly reduces ROS levels, eliminates DPPH free radicals, protects retinal pigment epithelial cells, and inhibits lipid peroxidation. Callistephin chloride can alleviate glutamate excitotoxicity, reduce neuronal apoptosis, and protect cerebellar granule neurons. Callistephin chloride can inhibit the proliferation and metastasis of breast cancer cells by inducing apoptosis^{[1][2][3][4][5][6]}. In Vitro:Callistephin chloride (5-100 μg/mL) significantly alters the morphology of red blood cells, increases the density of the membrane's hydrophilic regions, and has no obvious effect on the hydrophobic regions of the membrane^[1].
Callistephin chloride (5-50 μg/mL, 30 min) inhibits erythrocyte membrane lipid oxidation induced with UVC and AAPH radical with IC₅₀s of 17.7 and 5.8 μg/mL^[1].
Callistephin (0-400 μM μM, 24 h) chloride enhances the protective effects of Isoflurane by modulating engulfment and apoptosis in C8‑B4 cells involved in the modulation of inducible nitric oxide synthase, cytochrome c oxidase subunit 2, tumor necrosis factor α and nuclear factor κ B^[2].
Callistephin (0.1-1 μg/mL, 30 min) chloride can effectively protect retinal pigment epithelium (RPE) cells by decreasing intracellular ROS and increasing mitochondrial redox activity in blue-light irradiated ARPE-19 cells^[3].
Callistephin (100 μM μM, 24 h) chloride significantly protects cerebellar granule neurons (CGNs) from the toxicity of glutamate but has no capacity to defend neurons from nitric oxide (NO)-induced apoptosis^[4].
Callistephin-rich extracts (0-200 μg/mL, 24-72 h) chloride inhibits the proliferation of MCF-7 cells, induces cell apoptosis, and exhibits DPPH radical scavenging activity and iron ion reduction ability^[5].
In Vivo:Callistephin (3 mg/kg, i.p., single dose) chloride increases the expression of neuroD induced by Aβ in rats^[6].