Taurodeoxycholate (1.25-5 mg/kg, p.o., 6 days) sodium salt ameliorates dextran sodium sulfate (DSS)-induced colitis in mice[9].
Taurodeoxycholate sodium salt (Taurodeoxycholic acid form, 50 mg/kg; i.p.; once daliy for 34 d) prevents neuropathology and associated behavioral deficits in the 3-nitropropionic acid rat model of Huntington's disease (HD) [10].
Taurodeoxycholate sodium salt (Taurodeoxycholic acid form, 500 mg/kg; s.c.; once every 3 d for 7 weeks) leads to a significant reduction in striatal neuropathology of the R6/2 transgenic HD mouse[11].
Taurodeoxycholate (0.5 mg/kg; i.v., once) sodium salt confers protection to C57BL/6N mice with sepsis, but does not protect TGR5 KO mice under sepsis[12].
| Animal Model: | A mouse colitis model (fed with 3% (w/v) DSS in drinking water for the first seven days and then switched to normal drinking water for an additional two days)[9] |
| Dosage: | 1.25, 2.5, and 5 mg/kg |
| Administration: | Oral gavage (p.o.), from day 3 to day 8, once a day |
| Result: | Prevented loss of body weight, shortening of the colon, production of pro-inflammatory cytokines, infiltration of pro-inflammatory cells, and mucosal ulceration in the colon.
|
| Animal Model: | Huntington's disease model in mouse[10] |
| Dosage: | 50 mg/kg |
| Administration: | Intraperitoneal injection; once daliy for 34 d, injected 3-NP at 6 hr after Taurodeoxycholic acid treatment |
| Result: | Reduced striatal atrophy, decreased striatal apoptosis, as well as fewer and smaller size ubiquitinated neuronal intranuclear huntingtin inclusions.
Significantly improved locomotor and sensorimotor deficits.
|
| Animal Model: | C57BL/6N mice, Lipopolysaccharides (HY-D1056) injection model of sepsis[12] |
| Dosage: | 0.5 mg/kg |
| Administration: | Intravenous injection, 30 min or 24 h after LPS injection |
| Result: | Improved the survival rate of mice with sepsis.
Decreased liver and kidney damage in septic mice.
Ameliorated systemic inflammation and normalized blood pressure in septic mice.
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