Tauroursodeoxycholate (TUDCA) activates mitogen-activated phosphophosphatase 1 (MKP-1) through PKCα and suppresses ERK phosphorylation, ultimately decreasing the survival and migration of vascular smooth muscle cells (VSMC). Tauroursodeoxycholate suppresses ERK through Ca2+-induced PKCα translocation Tauroursodeoxycholate (200 μM) can restore VSMC decreased by Tauroursodeoxycholate (200 μM), consequently limiting the proliferation and migration of VSMC. activity, which implies that the anti-stress impact of Tauroursodeoxycholate depends on the expression of MKP-1 [1].

Using transferase dUTP nick cleavage labeling (TUNEL) and immunohistochemistry for tumescent cell nuclear factor (PCNA) assays, the effects of tauroursodeoxycholate (TUDCA) on VSMC swelling and inflammation in vivo were investigated. Caspase 3 activity in damaged tissue was experimentally boosted by tauroursodeoxycholate (10, 50, and 100 mg/kg), and tauroursodeoxycholate caused mutations in VSMCs in the neointima. One week following the injury, the phosphorylation levels of ERK and MMP-9 expression were measured using the injured tissue and compared with normal controls. Injuries to balloons raise MMP-9 production and phosphorylation of ERK in the tissue. In a mimetic regulatory approach, tauroursodeoxycholate (10, 50, and 100 mg/kg) suppresses the phosphorylation of ERK and MMP-9 [1]. The bile acid tauodeoxycholate (TUDCA) is hydrophilic. Tauodeoxycholate decreases endoplasmic reticulum intermediate cells and the pancreas, which enhances liver function as a cytoprotective agent and may prevent hepatocellular cancer. When tauodeoxycholate is administered to Ang II-induced ApoE-/-mice, it dramatically lowers the expression of Andrew molecules, including eIF2α, caspase-3, caspase-12, C/EBP homologous protein, c-Jun N-terminator protein (JNK), activating transcription factor 4 (ATF4), X-box binding protein (XBP), and JNK. This effect is significant (p<0.05). In ApoE-/-mice, tauroursodeoxycholate decreases the abdominal aorta caused by angiotensin II. 0.5 g/kg/day of tauroursodeoxycholate was administered to Ang II-induced ApoE-/- mice (ER pair). ..There was no difference in the total cholesterol level (663.6±88.7 mg/dL vs 655.7±65.4 mg/dL; p>0.05) or systolic blood pressure (141.3±5.6 mmHg vs 145.9±8.9 mmHg; p>0.05) between the Tauroursodeoxycholate group and the AAA model group. Furthermore, the Tauroursodeoxycholate group's AAA lesion area was less than the AAA model group's (0.37±0.03 mm2 vs. 1.51±0.06 mm; p<0.05) in comparison to the AAA model group. )[2].

[1]. Kim SY, et al. Tauroursodeoxycholate (TUDCA) inhibits neointimal hyperplasia by suppression of ERK viaPKCα-mediated MKP-1 induction. Cardiovasc Res. 2011 Nov 1;92(2):307-16.
[2]. Qin Y, et al. Tauroursodeoxycholic Acid Attenuates Angiotensin II Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-deficient Mice by Inhibiting Endoplasmic Reticulum Stress. Eur J Vasc Endovasc Surg. 2017 Mar;53(3):337-345

C26H49NO8S

535.7342

14605-22-2

Tauroursodeoxycholate sodium;35807-85-3;Tauroursodeoxycholate-d4 sodium;2410279-95-5;Tauroursodeoxycholate dihydrate;117609-50-4;Tauroursodeoxycholate-d5;1207294-25-4;Tauroursodeoxycholate-d4;2410279-94-4;Tauroursodeoxycholate-d4-1;2573035-17-1

S(C([H])([H])C([H])([H])N([H])C(C([H])([H])C([H])([H])[C@@]([H])(C([H])([H])[H])[C@@]1([H])C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])[C@]([H])(C([H])([H])[C@]4([H])C([H])([H])[C@@]([H])(C([H])([H])C([H])([H])[C@]4(C([H])([H])[H])[C@@]3([H])C([H])([H])C([H])([H])[C@@]21C([H])([H])[H])O[H])O[H])=O)(=O)(=O)O[H].O([H])[H].O([H])[H]

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~100.06 mM)
H2O : ~12.5 mg/mL (~25.02 mM)

Solubility in Formulation 1: 100 mg/mL (200.12 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

---

 (Please use freshly prepared in vivo formulations for optimal results.)