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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Ishimoto H, Matsuoka I, Nakanishi H, Nakahata N

Department of Pharmacology, Fukushima Medical College, Japan.

Gen Pharmacol. 1996 Mar;27(2):313-17. doi: 10.1016/0306-3623(95)02018-7.

ATP, bradykinin (BK), and A-23187 activated the generation of prostaglandin (PG) E2 and thromboxane (TX) B2 in rabbit astrocytes, but not in human astrocytoma cells (1321N1). 2. In human astrocytoma cells, ATP, BK, and A-23187 could not release [3H]arachidonic acid (AA) from [3H]AA-labeled cells and exogenous AA was not converted to TXB2 and PGE2, suggesting the lack of phospholipase (PL) A2 and cyclooxygenase activities in 1321N1 human astrocytoma cells, although they express TXA2 receptors. 3. In rabbit astrocytes, ATP and BK, but not A-23187, showed increased accumulation of inositol phosphates, indicating that an increase in intracellular Ca2+ concentration alone would not be enough to activate PLC. Furthermore, indomethacin, a cyclooxygenase inhibitor, partially attenuated ATP-induced phosphoinositide hydrolysis, indicating that cyclooxygenase product(s) would secondarily activate PLC in response to ATP.

三磷酸腺苷（ATP）、缓激肽（BK）和A - 23187可激活兔星形胶质细胞中前列腺素（PG）E2和血栓素（TX）B2的生成，但对人星形细胞瘤细胞（1321N1）无此作用。2. 在人星形细胞瘤细胞中，ATP、BK和A - 23187不能从[3H]花生四烯酸（AA）标记的细胞中释放[3H]AA，且外源性AA也不能转化为TXB2和PGE2，这表明1321N1人星形细胞瘤细胞缺乏磷脂酶（PL）A2和环氧化酶活性，尽管它们表达血栓素A2受体。3. 在兔星形胶质细胞中，ATP和BK可使肌醇磷酸积累增加，而A - 23187则不能，这表明仅细胞内Ca2+浓度升高不足以激活磷脂酶C（PLC）。此外，环氧化酶抑制剂吲哚美辛可部分减弱ATP诱导的磷酸肌醇水解，这表明环氧化酶产物会继发激活PLC以响应ATP。

Ishimoto H, Matsuoka I, Nakanishi H, Nakahata N

Department of Pharmacology, Fukushima Medical College, Japan.

Gen Pharmacol. 1996 Mar;27(2):313-17. doi: 10.1016/0306-3623(95)02018-7.

ATP, bradykinin (BK), and A-23187 activated the generation of prostaglandin (PG) E2 and thromboxane (TX) B2 in rabbit astrocytes, but not in human astrocytoma cells (1321N1). 2. In human astrocytoma cells, ATP, BK, and A-23187 could not release [3H]arachidonic acid (AA) from [3H]AA-labeled cells and exogenous AA was not converted to TXB2 and PGE2, suggesting the lack of phospholipase (PL) A2 and cyclooxygenase activities in 1321N1 human astrocytoma cells, although they express TXA2 receptors. 3. In rabbit astrocytes, ATP and BK, but not A-23187, showed increased accumulation of inositol phosphates, indicating that an increase in intracellular Ca2+ concentration alone would not be enough to activate PLC. Furthermore, indomethacin, a cyclooxygenase inhibitor, partially attenuated ATP-induced phosphoinositide hydrolysis, indicating that cyclooxygenase product(s) would secondarily activate PLC in response to ATP.

三磷酸腺苷（ATP）、缓激肽（BK）和A - 23187可激活兔星形胶质细胞中前列腺素（PG）E2和血栓素（TX）B2的生成，但对人星形细胞瘤细胞（1321N1）无此作用。2. 在人星形细胞瘤细胞中，ATP、BK和A - 23187不能从[3H]花生四烯酸（AA）标记的细胞中释放[3H]AA，且外源性AA也不能转化为TXB2和PGE2，这表明1321N1人星形细胞瘤细胞缺乏磷脂酶（PL）A2和环氧化酶活性，尽管它们表达血栓素A2受体。3. 在兔星形胶质细胞中，ATP和BK可使肌醇磷酸积累增加，而A - 23187则不能，这表明仅细胞内Ca2+浓度升高不足以激活磷脂酶C（PLC）。此外，环氧化酶抑制剂吲哚美辛可部分减弱ATP诱导的磷酸肌醇水解，这表明环氧化酶产物会继发激活PLC以响应ATP。