Journal of Hebei Medical College for Continuing Education ›› 2026, Vol. 43 ›› Issue (1): 1-10.DOI: 10.3969/j.issn.1674-490X.2026.01.001

   

Regulatory effect of taurine on the expression of aquaporin 4(AQP4)in the brain and its therapeutic role in bilirubin encephalopathy

FAN Ping1, GAO Yuyang2, XIAO Zeyu3, DONG Zelin3, GUO Keyun3, MAO Binyi3, CHEN Yuxiao2, ZHANG Yuhan2, GAN Shengwei3,4   

  1. 1. Department of Obstetrics and Gynecology, Chongqing University Affiliated Renji Hospital (the Fifth People's Hospital of Chongqing), Chongqing 401336, China; 2. University of Leicester Joint Institute, Chongqing Medical University, Chongqing 400016, China; 3. National Demonstration Center for Experimental Basic Medical Education Teaching, Chongqing Medical University, Chongqing 400016, China; 4. Department of Human Anatomy, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, China
  • Received:2025-11-25 Published:2026-03-10

Abstract: Objective To evaluate the regulatory effect of exogenous taurine(Tau)on the expression of aquaporin 4(AQP4)in the parietal cerebral cortex of a rat pup model of bilirubin encephalopathy(BE)and clarify its therapeutic effect on BE and the underlying molecular mechanism. Methods Neonatal SD rats weighing 10-15 g were randomly divided into three groups: sham operation group(Sham group), bilirubin encephalopathy group(BE group), and taurine treatment group(BE+Tau group). The BE group was intraperitoneally injected with taurine solvent, followed by cisterna magna injection of bilirubin(20 mg/kg body weight)4 hours later to induce the BE model. The BE+Tau group was first intraperitoneally injected with taurine(15 mg/kg body weight), and bilirubin was injected via cisterna magna 4 hours later. The Sham group was first administered with taurine solvent via intraperitoneal injection, followed by an injection of bilirubin solvent via cisterna magna at 4 hours post the initial treatment. After modeling, the neurobehavioral manifestations of rats in each group were observed. At 24 hours after modeling, brain tissues were harvested from all rat pups. HE staining and Nissl staining were used to assess the degree of neuronal damage. The water content of brain tissue was measured by the dry-wet weight method. Rhodamine B isothiocyanate leakage assay was used to determine the type of cerebral edema in BE. Western blot was employed to detect the expression level of AQP4 in the parietal cortex. Results Compared with the Sham group, rats in the BE group showed obvious neurobehavioral abnormalities such as opisthotonus and unsteady crawling, significantly increased brain water content, obvious neuronal edema and damage, and the type of cerebral edema was cytotoxic edema. Additionally, the expression of AQP4 in the parietal cortex was significantly upregulated. Compared with the BE group, the neurobehavioral abnormalities of rats in the BE+Tau group were significantly alleviated, the brain water content was decreased, the neuronal edema and damage were improved, and the upregulation of AQP4 expression induced by unconjugated bilirubin(UCB)was significantly inhibited. Conclusion Exogenous taurine can delay the occurrence of cytotoxic edema, alleviate neuronal damage, and thereby inhibit the progression of BE by suppressing the UCB-induced upregulation of AQP4 expression in the parietal cortex of BE neonatal rats.

Key words: taurine, bilirubin encephalopathy, aquaporin 4, cytotoxic edema

CLC Number: