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Tanshi IIA sulfonate sodium

CAS No. : 69659-80-9

MCE 站：Tanshi IIA sulfonate sodium

产品活性：Tanshi IIA sulfonate sodium 是 tanshi IIA 的衍生物，为 SOCE 的抑制剂，用于心血管疾病的研究。

研究领域：Membrane Transporter/Ion Channel

作用靶点：CRAC Channel

In Vitro: Sodium Tanshi IIA sulfonate (12.5 μM) inhibits hypoxia-induced PKG and PPAR-γ downregulation in PASMCs and distal pulmonary arteries of rats. The suppressive effects of Sodium Tanshi IIA sulfonate on TRPC1 and TRPC6 expression in hypoxic PASMCs can be prevented by specific knockdown PKG or PPAR-γ. The suppressive effects of Sodium Tanshi IIA sulfonate 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 Sodium Tanshi IIA sulfonate on proliferation in hypoxic PASMCs. PPAR-γ agonist promotes the protective role of Sodium Tanshi IIA sulfonate on basal [Ca²⁺]i and SOCE in hypoxic PASMCs. Sodium tanshi IIA sulfonate 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±14.6 ?M and 0.9±0.1 nmol/mg protein/min, respectively, for the HLMs and 7.5±1.4 ?M and 6.8±0.3 nmol/nmol P450/min, respectively, for CYP3A4. CYP1A2, CYP2A6, CYP2C9, CYP2D6, CYP2E1, and CYP2C19 show minimal or no effects on the metabolism of STS. Sodium Tanshi IIA sulfonate inhibits the activity of CYP3A4 in a dose-dependent manner in the HLMs and CYP3A4 isoform. Sodium Tanshi IIA sulfonate primarily inhibits the activities of CYP3A4 in vitro, and Sodium Tanshi IIA sulfonate has the potential to perpetrate drug-drug interactions with other CYP3A4 substrates.

In Vivo: Sodium Tanshi IIA sulfonate (10 mg/kg, 20 mg/kg) and Donepezil shorten escape latency, increase crossing times of the original position of the platform, and increase the time spent in the target quadrant. Sodium Tanshi IIA sulfonate decreases the activity of acetylcholinesterase (AChE) and increases the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice. Sodium Tanshi IIA sulfonate increases the activity of superoxide dismutase (SOD) and decreases the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in hippocampus and cortex. Sodium Tanshi IIA sulfonate prevention (30 mg/kg/day) alleviates hypoxia-induced characteristic changes in chronic hypoxia PH rat model. Sodium Tanshi IIA sulfonate (20, 10, and 5 mg/kg, i.p.) effectively prevents peritoneal adhesion without affecting anastomotic healing in the rats. Compared with the adhesion model group, the Sodium Tanshi IIA sulfonate-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.

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