Rb1, short for Retinoblastoma protein 1, is encoded by a well-known tumor suppressor gene. Since its discovery decades ago, it has served as a prototype for tumor genetic research. RB1 plays a key role in restraining cell cycle entry, and its pathway alterations are involved in most human cancers, often with prognostic value. It also regulates numerous cellular processes and impacts cell response to various stimuli, ultimately determining cell fate [2,3,4].

In ischemic stroke, ginsenoside Rb1 (not to be confused with the Rb1 gene, but an interesting related compound) inhibits astrocyte activation and promotes the transfer of astrocytic mitochondria to neurons. In response to oxygen-glucose deprivation and reperfusion, astrocytes produce reactive oxygen species (ROS), which is blocked by ginsenoside Rb1. It inhibits NADH dehydrogenase in mitochondrial complex I, blocking reverse electron transport-derived ROS production, thus inactivating astrocytes and protecting mitochondria. CD38 knockdown in the cerebral ventricles of an ischemic mouse brain model diminished the neuroprotective effects of ginsenoside Rb1, indicating the role of astrocyte mitochondrial transfer [1].

In summary, Rb1 is a crucial tumor suppressor gene with a key role in cell cycle regulation and is involved in various cellular processes. The study of ginsenoside Rb1 in an ischemic mouse model provides insights into potential neuroprotective strategies related to Rb1-associated pathways in ischemic brain injury, highlighting the importance of understanding Rb1-related mechanisms for treating such diseases [1,2,3,4].