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BACKGROUND: The aging and lesions of the intervertebral disc are closely related to the lack of nutritional blood supply to the disc. Aquaporin plays an important role in the nutritional supply to the intervertebral discs, but the specific mechanism has not been fully defined. OBJECTIVE: To study the mechanism of Yaobishu on degenerated intervertebral disc in rabbits based on the changes of aquaporin (AQP) 1 and AQP3 protein expression. METHODS: Thirty-six New Zealand white rabbits were randomly divided into model group, low-dose Yaobishu group and high-dose Yaobishu group. Animal models of lumbar intervertebral disc prolapse were prepared through an injection of normal saline into L4/5 and L5/6 segments. The model group was intragastrically given normal saline 5 mL/kg per day, the low-dose group was intragastrically given Yaobishu 5 mL/kg per day, and the high-dose group was intragastrically given Yaobishu 10 mL/kg per day, twice a day, for 21 days. After 6 weeks of treatment, the intervertebral discs were taken for anatomical and histological observation using hematoxylin-eosin staining. Expression of AQP1 and AQP3 in the nucleus pulposus at protein and mRNA levels was quantified by RT-PCR and western blot assay. RESULTS AND CONCLUSION: In all the three groups, the annulus fibrosus was destroyed, abnormal cartilage tissue appeared, and the nucleus pulposus was reduced in number. Severest degeneration of the intervertebral disc was found in the model group, followed by the low-dose Yaobishu and high-dose Yaobishu groups in turn. The expression of AQP1 and AQP3 mRNA and protein in the high-dose Yaobishu group and low-dose Yaobishu group increased significantly after 6 weeks of treatment (P < 0.05), while the expression in the model group showed no significant difference before and after treatment (P > 0.05). There were significant differences in the expression of AQP1 and AQP3 mRNA and protein among the three groups (P < 0.05). Therefore, Yaobishu may alleviate the degeneration of the rabbit intervertebral disc by increasing the expression of AQP1 and AQP3. [ABSTRACT FROM AUTHOR]