This study was conducted to evaluate the effect of pyridoxine on the development of hair follicles in Rex rabbits and the underlying molecular mechanism. Two hundred 3-month-old Rex rabbits were randomly divided into 5 groups and fed diets supplemented with 0, 5, 10, 20, or 40 mg/kg pyridoxine. The hair follicle density on the dorsal skin and the gene and protein expression levels of components of the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB or Akt), Wnt, Notch and bone morphogenetic protein (BMP) signalling pathways were measured. In addition, free hair follicles were isolated from Rex rabbits and cultured with pyridoxine in vitro to measure hair shaft growth. Furthermore, dermal papilla cells (DPC) were isolated from the skin of Rex rabbits and cultured with pyridoxine in vitro to measure the gene and protein expression levels of components of the PI3K/Akt, Wnt, Notch and BMP signalling pathways. The results showed that the addition of dietary pyridoxine significantly increased the total follicle density, secondary follicle density, and secondary-to-primary ratio (S/P, P < 0.05), that the growth ratio of hair stems was promoted by pyridoxine in basic culture medium, and that the growth length of tentacle hair follicles cultured in the pyridoxine group was longer than that in the control group (P < 0.05). In addition, pyridoxine changed the DPC cycle progression and promoted cell proliferation, and appropriate concentrations of pyridoxine (10 and 20 μmol/L) significantly inhibited cell apoptosis (P < 0.05). Pyridoxine significantly affected the gene expression of components of the PI3K/Akt, Wnt and Notch signalling pathways in the skin and DPC of Rex rabbits (P < 0.05), increased the levels of phosphorylated catenin beta 1 (CTNNB1) and Akt, and decreased the level of phosphorylated glycogen synthase kinase 3 beta (GSK-3β) (P < 0.05). Therefore, the molecular mechanism by which pyridoxine promotes hair follicle density in Rex rabbits probably occurs through activation of the PI3K/Akt, Wnt and Notch signalling pathways, prolonging hair follicle growth and delaying the onset of telogen.

本研究旨在评估吡哆醇对雷克斯兔毛囊发育的影响及其潜在的分子机制。将 200 只 3 个月大的雷克斯兔随机分为 5 组，分别饲喂添加 0、5、10、20 或 40 mg/kg 吡哆醇的饮食。测量背部皮肤上的毛囊密度以及磷酸肌醇 3-激酶 (PI3K)/蛋白激酶 B（PKB 或 Akt）、Wnt、Notch 和骨形态发生蛋白 (BMP) 信号通路组分的基因和蛋白质表达水平. 此外，从雷克斯兔中分离出游离毛囊并在体外与吡哆醇一起培养以测量毛干生长。此外，从雷克斯兔的皮肤中分离出真皮乳头细胞 (DPC)，并在体外与吡哆醇一起培养，以测量 PI3K/Akt、Wnt、Notch 和 BMP 信号通路组分的基因和蛋白质表达水平。结果表明，饮食中添加吡哆醇显着增加了总卵泡密度、次级卵泡密度和次级与初级比率（S/P，P  < 0.05），表明基础培养基中吡哆醇促进毛茎的生长，吡哆醇组培养的触手毛囊生长长度长于对照组（P  < 0.05）。此外，吡哆醇改变DPC循环进程并促进细胞增殖，适当浓度的吡哆醇（10和20μmol/L）显着抑制细胞凋亡（P  < 0.05）。吡哆醇显着影响雷克斯兔皮肤和DPC中PI3K/Akt、Wnt和Notch信号通路组分的基因表达（P < 0.05)，增加磷酸化连环蛋白 1 (CTNNB1) 和 Akt 的水平，降低磷酸化糖原合酶激酶 3 β (GSK-3β) 的水平 ( P  < 0.05)。因此，吡哆醇促进雷克斯兔毛囊密度的分子机制可能是通过激活 PI3K/Akt、Wnt 和 Notch 信号通路，延长毛囊生长和延迟休止期开始。