Objective:To preliminarily investigate the effects of tetramethylpyrazine(TMP)on expressions of aquaporin1

5 in lipopolysaccharide(LPS)-induced lung injury in rats. Methods:Thirty-two healthy male SPF grade SD rats were randomly divided into the normal control group(group C)

the TMP intervention group(group T)

the LPS stimulation group(group L) and the TMP treatment group(LT group)

with eight rats in each group. Rats in the group L were given LPS(6 mg/kg)through tail vein injection

rats in group T were given TMP(100 mg/kg)through intraperitoneal injection

and rats in group LT were given LPS for 1 h followed by TMP(100mg/kg)through intraperitoneal injection immediately. After 8 hours

all rats were anesthetized and sacrificed

with lung tissue specimens harvested. Wet/dry ratio(W/D)of the lung tissue was detected. In addition

hematoxylin-eosin(HE) staining was performed to observe the lung tissue morphology;Quantitative real-time PCR(q RT-PCR)was used to detect the AQP1 m RNA and AQP5 m RNA levels of the lung tissue homogenate. In addition

immunohistochemistry and Western blot were used to detect the protein expression of AQP1 and AQP5 in the lung tissue. Results:After HE staining of the lung tissue sections

the lung tissue was integral and clear in its structure in group C and T under light microscope. Alveoli were disorderly in structures

the diffuse alveolar septa were thickened

and alveolar inflammatory cell infiltration

hemorrhage and edema were observed in group L. While the LT group had milder pathological manifestations than group L. The average W/D ratio of the lung tissue in group L(5.577±0.243)was higher than that of each of the other three groups significantly(P<0.01). Compared with group C and T(3.430±0.251、3.251±0.142)

the W/D ratio in the group LT(4.384±0.236)was increased

and the difference was significant(P<0.01). The results of q RT-PCR showed that the levels of AQP1 RNA and AQP5 RNA in group T(1.462±0.080

1.267±0.063)were higher than those in group C(1.160±0.229

0.940±0.087)and the levels in group L(0.607±0.203

0.139±0.046)were down-regulated. Meanwhile

the levels in group LT(0.848±0.071

0.314±0.134)were higher than those in group L(P<0.05). The results of immunohistochemistry(C group:2.096±0.114

2.285±0.266;T group:3.253±0.149

3.790±0.308;L group:1.133±0.202

1.068 ±0.221;LT group:1.562 ±0.085

1.647±0.239)and Western blot(C group:1.443±0.103

1.278±0.061;T group:1.667±0.087

1.644±0.102;L group:0.974±0.090

0.529±0.100;LT group:1.179±0.051

0.805±0.082)were consistent with those of q RT-PCR(P<0.05). Conclusion:TMP can exhibit positive protective effects by mitigating LPS-induced pulmonary edema in ARDS effectively

and the mechanism may be associated with the upregulation of the expressions of AQP1 and AQP5.