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Updated: Dec 12, 2025
Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
Published on: February 10, 2015
Curcumin prevents cognitive deficits in the bile duct ligated rats
Somayeh Baghbaderani1, Mehrdad Hashemi1, Mohaddaseh Ebrahimi-Ghiri2
1Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Rationale:
Bile duct ligation (BDL) in rodents can cause impaired liver function and cognition deficits. Curcumin has shown a preventive and therapeutic role in memory impairment.
Objectives:
Therefore, this study aimed to explore the effect of curcumin on the performance of male adult Wistar rats that underwent BDL, a model of hepatic encephalopathy (HE) in the Morris water maze (MWM).
Methods:
Four weeks after surgery, sham (manipulation of common bile duct without ligation) and BDL rats underwent the MWM test.
Results:
The representative data showed that BDL rats exhibited impairments in spatial learning and reference memory in the MWM compared with the sham rats. Treatment of BDL rats with curcumin (40 mg/kg, i.p., for 4 weeks) prevented these impairments, while it did not affect spatial learning and memory in the sham rats, by itself. Curcumin increased expression levels of the pro-survival B cell lymphoma extra-large (Bcl-xL) gene and two genes involved in mitochondrial function, peroxisome proliferative-activated receptor-γ co-activator 1α (PGC-1α) and mitochondrial transcription factor A (TFAM), in the hippocampus of BDL rats compared with the vehicle-treated sham or BDL rats, while it decreased the pro-apoptotic Bcl-2-associated X protein (Bax) gene expression level. BDL up-regulated Bax and down-regulated TFAM, by itself. Furthermore, curcumin reduced the mRNA level of Bax, while it increased Bcl-2 and TFAM mRNA levels.
Conclusions:
These findings demonstrate the beneficial effect of curcumin on cognitive function in BDL rats of the HE model. The curcumin effect may be related to mitochondrial function improvement in the HE.
