Procyanidin C1  别名：PCC1; 原花青素C1

Procyanidin C1 (PCC1) 是一种天然多酚，可造成 DNA 损伤，细胞周期停滞，诱导凋亡 (apoptosis)。Procyanidin C1 降低癌细胞中 Bcl-2 的蛋白水平，增强 BAX，caspase 3 和 9 的表达。Procyanidin C1 (27.85 和 66.41 μL) 在 MCF-7 和 MDA-MB-231 癌细胞中诱导显著的 DNA 损伤。Procyanidin C1 (45 μg/mL；72 h) 降低 Bcl-2 的表达水平，增加 BAX 的表达水平，增加 caspase 3 和 9 的活性，诱导细胞凋亡 MCF-7 和 MDA-MB-231 癌细胞。

原花青素 C1 (20 mg/kg；腹腔注射；第一次 MIT 给药后 2 周，然后每两周给药一次) 促进肿瘤消退。原花青素 C1 (20 mg/kg；口服；持续 3 d) 可延长老年小鼠的寿命。

使用方法（仅供参考，整理自公开文献）

Senescent cell clearance and lifespan studies

For age-related studies, WT C57BL/6J male mice were maintained in a specific pathogen-free facility at 22–25 °C under a 12-h–12-h light–dark cycle (lights on from 08:00 to 20:00) with free access to food (standard mouse diet, LabDiet 5053) and water provided ad libitum. The experimental procedure was approved by the IACUC at Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, with all animals treated in accordance with the guidelines for animal experiments defined by the IACUC.

Mice were sorted by body weight from low to high, and pairs of mice were selected according to similar body weights. Either control cell or senescent cell transplant treatments were assigned to every other mouse using a random number generator, with the intervening mice assigned to the other treatment to allow mice transplanted with control and senescent cells to be matched by weight. After acclimation in the animal facility at Shanghai Institute of Nutrition and Health, mice aged 5 months were subcutaneously transplanted with MEFs (0.5 × 10⁶ cells per side) and treated immediately with vehicle or PCC1 (prepared in ethanol–polyethylene glycol 400–Phosal 50 PG at 10:30:60, 20 mg per kg) for 1 week (i.p. injection once every 3 d) before bioluminescence imaging assays. Physical function tests were performed 1 month after bioluminescence imaging at the age of approximately 25 weeks. The first death occurred approximately 3 months after the last physical function test. For treatment-delayed mice that received cell transplantation, a first wave of physical function tests was conducted 5 weeks after cell transplantation. Animals were then subjected to treatment with vehicle for 5 d (for those with control cells as the first group) or vehicle or PCC1 for 5 d (for those with senescent cells, as the second and third groups, respectively) (i.p. injections were performed consecutively for each condition once every 5 d). Mice were maintained for 2 weeks, after which the second wave of physical function assays was conducted. For mid-age studies, 17-month-old C57BL/6J mice were implanted with control or senescent MEF cells and underwent treatment with vehicle or PCC1. Administration was performed once biweekly, and animals were measured for survival within a 1-year time frame after cell implantation.

For senolytic studies of natural ageing, 20-month-old WT C57BL/6J mice (males) without transplantation were used and were sorted according to their body weight and randomly assigned to vehicle or PCC1 treatment. Animals were treated once every 2 weeks in an intermittent manner for 4 months before physical tests were performed at 24 months of age. For senolytic trials pertaining to lifespan extension at advanced age, we used animals at a very old age. Starting at 24–27 months of age (equivalent to a human age of 75–90 years), mice (both sexes) were treated once every 2 weeks (biweekly) with vehicle or PCC1 by oral gavage (20 mg per kg) for three consecutive days. Some mice were moved from their original cages during the study to minimize single cage-housing stress. In each case, RotaRod (TSE Systems) and hanging tests were chosen for monthly measurement of maximal speed and hanging endurance, respectively, as these tests are considered sensitive and noninvasive. Mice were euthanized and scored as having died if they exhibited more than one of the following signs: (1) unable to drink or eat, (2) reluctant to move even with stimulus, (3) rapid weight loss, (4) severe balance disorder or (5) bleeding or ulcerated tumour. No mouse was lost due to fighting, accidental death or dermatitis. The Cox proportional-hazard model was used for survival analyses.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8688144/