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Accumulating evidence has shown that tauroursodeoxycholic acid (TUDCA) is neuroprotective in different animal models of neurological diseases. However, whether TGR5 agonist TUDCA can improve lipopolysaccharide (LPS)-induced cognitive impairment in mice is less clear. Using a model of cognitive impairment with LPS (2.0 μg) we investigated the effects of TUDCA (200 or 400 μg) on cognitive dysfunction and neurotoxicity in mice. Both Morris water maze and Y-maze avoidance tests showed that TUDCA treatment significantly alleviated LPS-induced behavioral impairments. More importantly, we found that TUDCA treatment reversed TGR5 down-regulation, prevented neuroinflammation via inhibiting NF-κB signaling in the hippocampus of LPS-treated mice. Additionally, TUDCA treatment decreased LPS-induced apoptosis through decreasing TUNEL-positive cells and the overexpression of caspase-3, increasing the ratio of Bcl-2/Bax. TUDCA treatment also ameliorated synaptic plasticity impairments by increasing the ratio of mBDNF/proBDNF, the number of dendritic spines and the expression of synapse-associated proteins in the hippocampus. Our results indicated that TUDCA can improve cognitive impairment and neurotoxicity induced by LPS in mice, which is involved in TGR5-mediated NF-κB signaling.
This article was published in the following journal.
Name: International immunopharmacology
To investigate the effect of tauroursodeoxycholic acid (TUDCA) on neurological impairment induced by acute cerebral infarction (ACI) and its relevant mechanism of action.
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The purpose of the present study is to determine if use of dietary supplement tauroursodeoxycholic acid enhances insulin-stimulated leg blood flow and glucose disposal.
OBJECTIVES: I. Determine the optimum dose of tauroursodeoxycholic acid (TUDCA) required to achieve maximal bioavailability for patients with cystic fibrosis-associated liver disease. II....
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A catatoxic steroid and microsomal enzyme inducer having significant effects on the induction of cytochrome P450. It has also demonstrated the potential for protective capability against acetaminophen-induced liver damage.
Specialized clothing or equipment worn for protection against health hazards. Personal Protective Equipment may include MASKS; RESPIRATORY PROTECTIVE DEVICES; HEAD PROTECTIVE DEVICES; EYE PROTECTIVE DEVICES; EAR PROTECTIVE DEVICES; PROTECTIVE CLOTHING; and protective footwear.
Glycolipid-anchored membrane glycoproteins expressed on cells of the myelomonocyte lineage including MONOCYTES; MACROPHAGES; and some GRANULOCYTES. They function as receptors for the complex of lipopolysaccharide (LPS) and LPS-binding protein.
A condition of low alertness or cognitive impairment, usually associated with prolonged mental activities or stress.
Persistent detrimental effects from treatment for a condition. Included are effects from surgery such as POSTOPERATIVE COMPLICATIONS, and from DRUG THERAPY, such as CHEMICALLY INDUCED DISORDERS, or other THERAPEUTICS. Failure to attain a desired outcome from treatment for the condition is not considered an adverse effect.