Objective    To study the expression of aquaporin8 (AQP8) in rat astrocytes under hypotonic stress.     Methods    Primarily cultured rat astrocytes

randomly divided into control group (280 to 320 mmol/L) and 3 hypotonic groups at the concentration of 268

254

and 240 mmol/L respectively

were exposed to hypotonic stress for 1

3

6

12

and 24 h

respectively. Viability of astrocytes was detected by MTT colorimetry. Expression of AQP8 at protein and  mRNA levels in astrocytes was detected by immunocytochemistry

immunofluorescence

and real time reverse transcription polymerase chain reaction (RT-PCR)

respectively.     Results    No significant change was observed in morphology and viability of astrocytes as well as in expression of AQP8 and its mRNA at different time points in control group. Edema of astrocytes was observed

the viability of astrocytes was decreased

and the expression of AQP8 at protein and mRNA levels was in a negative concentration-dependent and positive time-dependent manner. Immunocytochemistry showed that the expression of AQP8 in astrocytes was 0.258 3±0.009 8

0.280 0±0.010 9

0.281 7±0.007 5 respectively after astrocytes were exposed to hypotonic stress at different concentrations for 1 h and were 0.385  0± 0.010 9

0.406 7±0.007 0

0.425 0±0.010 4

respectively

for 24 h  (P0.05). RT-PCR showed that the expression of AQP8 in astrocytes was increased from 0.258 3±0.009 8

0.280 0±0.010 9

0.281 7±0.007 5 in 1 h after astrocytes were exposed to hypotonic stress at different concentrations to 0.385±0.010 9

0.406 7±0.007 0

0.425 0±0.010 4 in 24 h after exposure (P0.05）compared to the expression of betaactin mRNA

which was increased from 0.127 5±0.011 8，0.134 4±0.032 4

0.167 5±0.007 8 in 1 h after exposure to 3.278 0±0.121 2

5.410 4±0.104 1

8.351 0±0.288 0 respectively in 24 h after exposure (P0.05).     Conclusion    AQP8-mediated water molecule transport can lead to edema

structure and function injury of astrocytes under hypotonic stress. Increased AQP8 expression may be one of the important mechanisms underlying  the formation and development of astrocyte edema. 