Tetrandrine and thapsigargin release arachidonic acid from cells in culture and stimulate prostacyclin production in rat liver cells, but may do so by different pathways

Table 1 Effects of Diltiazem (50 μg/ml), Actinomycin D (1 μg/ml), EGTA (1 mM), KCl (100 mM), and BABTA/AM (16 μg/ml) on AA Release from HT-29 or C-9 Cells stimulated by TET or THAP.

Some biological effects*	Agent tested	Action of test agent	AA Release
			HT-29	C-9
TET	Diltiazem	Blocks L-type Ca²⁺ channels	NI	NI
Ion Channels	Actinomycin D	Inhibits RNA synthesis	NI	NI
Apoptosis	EGTA	Chelates extracellular Ca²⁺	NI	NI
Depolarization	100 mM KCl	Depolarizes	NI	NI
[Ca²⁺]_I	BAPTA/AM	Chelates [Ca²⁺]_i	NI	**
THAP	Diltiazem	Blocks L-type Ca²⁺ channels	NI	NI
Ion Channels	Actinomycin D	Inhibits RNA synthesis	↓	↓
Apoptosis	EGTA	Chelates extracellular Ca²⁺	↓	↓
Depolarization	100 mM KCl	Depolarizes	↓	↓
[Ca²⁺]_i	BAPTA/AM	Chelates [Ca²⁺]_I	↓	**

* = References in text
NI = No Inhibition (or stimulation)
↓ = Inhibition: statistically significant
** = BAPTA/AM (16 μg/ml) stimulates AA release (6.17 ± 0.088 (4)), MEM/BSA control vs (11.6 ± 0.322 (4)), BAPTA/AM (16 μg/ml). Thus, the effect of BAPTA/AM on C-9 cells is not recorded.