Li Ting, Zhang Youran, Zhu Baihui, Wu Chunfang, Chen Yong
Pharmazie. 2018 Oct 1;73(10):585-588. doi: 10.1691/ph.2018.8592.
Recent studies have shown that telmisartan (TMS) is effective for the protection against ischemia/brain damage in rat models. However, the specific underlying mechanism is poorly understood. In line with previous results, our data showed that TMS improves CBF and physiological variables, including pH, pCO2, pO2. Through CD31 immunofluorescence staining, reduction of blood vessel density was found in MCAO group, but TMS treatment could enhance the cerebral vascular density in the ischemic area. Meanwhile, TMS treatment could enhance the number of BrdU/lectin double-positive cells. Furthermore, the reduction of nestin-positive cells was identified in the brain of MCAO rats, while the number of nestin-positive cells was significantly increased after TMS administration. Furthermore, the expression of ERS-related proteins, including GRP78, CHOP/GADD153, Caspase12 was increased after MCAO, but was decreased after administration of TMS, thereby enhancing angiogenesis and neuron regeneration.
最近的研究表明，替米沙坦（TMS）在大鼠模型中对预防缺血/脑损伤有效。然而，其具体的潜在机制尚不清楚。与先前的结果一致，我们的数据表明，TMS可改善脑血流量和生理变量，包括pH值、二氧化碳分压、氧分压。通过CD31免疫荧光染色发现，大脑中动脉闭塞（MCAO）组血管密度降低，但TMS治疗可增加缺血区域的脑血管密度。同时，TMS治疗可增加5-溴脱氧尿嘧啶核苷（BrdU）/凝集素双阳性细胞的数量。此外，在MCAO大鼠脑中发现巢蛋白阳性细胞减少，而给予TMS后巢蛋白阳性细胞数量显著增加。此外，MCAO后内质网应激（ERS）相关蛋白，包括葡萄糖调节蛋白78（GRP78）、C/EBP同源蛋白（CHOP）/生长停滞和DNA损伤诱导蛋白153（GADD153）、半胱天冬酶12的表达增加，但给予TMS后表达降低，从而促进血管生成和神经元再生。
