Tanshinone IIA sulfonate (sodium)

Tanshinone IIA sulfonate (sodium) is a derivative of tanshinone IIA, which acts as an inhibitor of store-operated Ca²⁺ entry (SOCE), and is used to treat cardiovascular disorders. In Vitro:Tanshinone IIA (12.5 μM) sulfonate sodium inhibits hypoxia-induced PKG and PPAR-γ downregulation in PASMCs and distal pulmonary arteries of rats. The suppressive effects of Tanshinone IIA sulfonate sodium on TRPC1 and TRPC6 expression in hypoxic PASMCs can be prevented by specific knockdown PKG or PPAR-γ. The suppressive effects of Tanshinone IIA sulfonate sodium on basal calcium concentration and SOCE in hypoxic PASMCs can be reversed by specific knockdown of PKG or PPAR-γ. PKG-PPAR-γ signaling axis participates in the suppressive effects of Tanshinone IIA sulfonate sodium on proliferation in hypoxic PASMCs. PPAR-γ agonist promotes the protective role of Tanshinone IIA sulfonate sodium on basal [Ca²⁺]i and SOCE in hypoxic PASMCs^[2].
Tanshinone IIA sulfonate sodium inhibits the activity of CYP3A4 in a dose-dependent manner by the HLMs and CYP3A4 isoform. The K_M and Vmax values of STS are 54.8 μM and 0.9 nmol/mg protein/min, respectively, for the HLMs and 7.5 μM and 6.8 nmol/nmol P450/min, respectively, for CYP3A4. CYP1A2, CYP2A6, CYP2C9, CYP2D6, CYP2E1, and CYP2C19 show minimal or no effects on the metabolism of STS^[3].
Tanshinone IIA sulfonate sodium inhibits the activity of CYP3A4 in a dose-dependent manner in the HLMs and CYP3A4 isoform. Tanshinone IIA sulfonate sodium primarily inhibits the activities of CYP3A4 in vitro, and Tanshinone IIA sulfonate sodium has the potential to perpetrate drug-drug interactions with other CYP3A4 substrates^[4].
In Vivo:Tanshinone IIA (10 mg/kg, 20 mg/kg) sulfonate sodium and Donepezil shorten escape latency, increase crossing times of the original position of the platform, and increase the time spent in the target quadrant. Tanshinone IIA sulfonate sodium decreases the activity of acetylcholinesterase (AChE) and increases the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice. Tanshinone IIA sulfonate sodium increases the activity of superoxide dismutase (SOD) and decreases the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in hippocampus and cortex^[1].
Tanshinone IIA (30 mg/kg/day) sulfonate sodium prevention alleviates hypoxia-induced characteristic changes in chronic hypoxia PH rat model^[2].
Tanshinone IIA (20, 10, and 5 mg/kg, i.p.) sulfonate sodium effectively prevents peritoneal adhesion without affecting anastomotic healing in the rats. Compared with the adhesion model group, the Tanshinone IIA sulfonate sodium-treated groups show increased peritoneal lavage fluid tPA activity and tPA/PAI-1 ratio in the ischemic tissues with loared TGF-β1 and collagen I expressions in the ischemic tissues^[5].