目的：探讨加味桃红四物汤(MTSD)对视网膜Müller细胞rMC-1缺氧损伤的保护作用。

方法：用加味桃红四物汤含药血清干预缺氧条件下rMC-1细胞，随机分为正常对照组(21%O₂)、缺氧模型组(1%O₂)、含药血清低(1%O₂+5%含药血清)、中(1%O₂+10%含药血清)、高剂量组(1%O₂+15%含药血清)，CCK-8法检测细胞的活力，ELISA法检测血管内皮生长因子(VEGF)和色素上皮衍生因子(PEDF)分泌，Western blot检测磷酸化转录激活因子3(p-STAT3)、转录激活因子3(STAT3)和缺氧诱导因子-1α(HIF-1α)的蛋白表达，Real time PCR检测VEGF、PEDF、STAT3和HIF-1α的基因表达。

结果：在1%O₂条件下培养48h，rMC-1细胞活力较正常对照组明显受到抑制(P<0.05)，加味桃红四物汤含药血清低、中剂量组均可以改善rMC-1细胞缺氧48h的细胞存活率(P<0.05)，而高剂量组无改善作用(P>0.05)。加味桃红四物汤含药血清低、中剂量组均可减少缺氧条件下rMC-1细胞上清液VEGF的蛋白表达量(P<0.05)，但不能增加PEDF的蛋白含量(P>0.05)，对p-STAT3和HIF-1α在蛋白水平均有下调作用(P<0.05)，且低剂量组抑制作用优于中剂量(P<0.05)。加味桃红四物汤含药血清中剂量组对缺氧后rMC-1细胞STAT3的蛋白表达有上调作用(P<0.05)。加味桃红四物汤含药血清低、中剂量组对缺氧后rMC-1细胞VEGF基因表达均有下调作用(P<0.05)，对PEDF基因表达均有上调作用(P<0.05)，且低剂量组优于中剂量(P<0.05)； 并且加味桃红四物汤含药血清低剂量可下调缺氧后STAT3和HIF-1α的基因表达(P<0.05)。

结论：加味桃红四物汤含药血清可能通过抑制STAT3/HIF-1α通路，下调缺氧诱导的视网膜Müller细胞rMC-1的VEGF蛋白和基因表达，上调PEDF基因表达，减轻该细胞的缺氧损伤。

METHODS: Retinal Müller cells rMC-1 were interfered with the MTSD drug-containing serum under hypoxia condition, and were randomly divided into control group(21%O₂), hypoxia model group(1%O₂), MTSD drug-containing serum low-dose(1%O₂+5% medicated serum), medium-dose(1%O₂+10% medicated serum)and high-dose(1%O₂+15%medicated serum)groups. Cell viability was detected by CCK-8 method, and secretion of vascular endothelial growth factor(VEGF)and pigment epithelium derived factor(PEDF)was detected by ELISA. The protein expressions of p-STAT3, STAT3 and hypoxia-inducible factor-1α(HIF-1α)were detected by Western blot, and the gene expressions of VEGF, PEDF, STAT3 and HIF-1α were detected by real-time polymerase chain reaction(PCR).

RESULTS: The viability of rMC-1 cells was significantly inhibited when cultured at 1%O₂ for 48h compared with that of control group(P<0.05), while it was improved in both low and medium dose of MTSD groups(P<0.05). The viability of rMC-1 cells in high dose group was not improved in hypoxia condition(P>0.05). The low and medium doses of MTSD could reduce the protein expressions of VEGF in supernatant of rMC-1 cells under hypoxia condition(P<0.05), while the protein expressions of PEDF could not be increased(P>0.05). The above two dose groups down-regulated the protein levels of both p-STAT3 and HIF-1α(P<0.05), and the inhibition effect of low dose group was better than that of medium dose group(P<0.05). The medium dose of MTSD could up-regulate STAT3 protein level after hypoxia culture in rMC-1 cells(P<0.05). The low and medium doses of MTSD significantly down-regulated VEGF gene level(P<0.05)and up-regulated PEDF gene level after hypoxia culture in rMC-1 cells(P<0.05), and the function in the low dose group was superior to that in the medium dose group(P<0.05). The low dose of MTSD could down-regulate STAT3 and HIF-1α gene levels after hypoxia culture in rMC-1 cells(P<0.05).

CONCLUSION: Probably by inhibiting the STAT3/HIF-1α pathway, the drug-containing serum of MDST down-regulated the expression of VEGF protein and gene in hypoxia-induced retinal Müller cells, rMC-1, up-regulated the gene expression of PEDF, and alleviated the hypoxia injury to the cells.