Study on the hepatotoxicity and potential mechanism of gefitinib based on CYP450 in mice and AML12 cells.

Objectives: Gefitinib is mainly used for the treatment of non-small-cell lung cancer. Hepatotoxicity is one of the main side effects of gefitinib, and seriously affects the treatment process of the disease. However, the hepatotoxicity mechanism of gefitinib remains unclear.

Baicalin improves the energy levels in the prefrontal cortex of mice exposed to chronic unpredictable mild stress.

Depression is gradually becoming a primary mental disease threatening human health. Therefore, there is an urgent need to clarify the pathogenesis of depression and identify new effective natural antidepressants. This study aimed to investigate the antidepressant effects of baicalin and explore its potential mechanism in a mouse model of depression induced by chronic unpredictable mild stress (CUMS).

Baicalin ameliorates CUMS-induced depression-like behaviors through activating AMPK/PGC-1α pathway and enhancing NIX-mediated mitophagy in mice.

Mitochondrial dysfunction has been reported to be involved in the pathogenesis of depression, and mitophagy is a key pathway for mitochondrial quality control. This study aimed to investigate the effect of baicalin on mitophagy in the hippocampus of mice exposed to chronic unpredictable mild stress (CUMS) and explore its potential mechanism. After exposure to CUMS for 6 weeks, mice were given baicalin (20 mg/kg) or fluoxetine (20 mg/kg) by oral gavage for 4 weeks, and HT22 cells were injured by corticosterone (CORT) in vitro.

The antidepressant-like effect of formononetin on chronic corticosterone-treated mice.

Previous studies reported the neuroprotective effects of formononetin (FMN), however, whether it has antidepressant-like effects have not been reported. To evaluate the antidepressant-like effects of FMN, a mice model of depression was established by chronic corticosterone (CORT) injection. The serum corticosterone levels and hippocampal protein expression were detected by ELISA and Western blot.

Tandem mass tag-based quantitative proteomic analysis of the liver reveals potential protein targets of Xiaochaihutang in CUMS model of depression.

Depression is a global mental disorder disease and greatly threatened human health. Xiaochaihutang (XCHT) has been used successfully in treatment of depression for many years in China, but the mechanism is unclear. Using the chronic unpredictable mild stress (CUMS) mice model of depression, the present study aimed to reveal possible antidepressant mechanisms of XCHT from the perspective of liver by analyzing hepatic proteomics in mice.

Quantitative proteomic analysis of the liver reveals antidepressant potential protein targets of Sinisan in a mouse CUMS model of depression.

In traditional Chinese medicine, the role of the liver in depression is highly valued, and liver-relieving drugs, such as Sinisan, are often used to treat depression; however, the mechanism whereby these drugs work remains unclear. The present study aimed to reveal possible antidepressant mechanisms of Sinisan (SNS) by analyzing hepatic proteomics in chronic unpredictable mild stress (CUMS) mice. Using the CUMS mouse model of depression, the antidepressant effects of SNS were assessed by the sucrose preference test (SPT) and forced swimming test (FST).

Effects of resveratrol on the levels of ATP, 5-HT and GAP-43 in the hippocampus of mice exposed to chronic unpredictable mild stress.

Growing evidence suggested that energy deficiency might be involved in the pathophysiological mechanism of depression. Energy deficiency, mainly results from mitochondrial damage, can lead to the dysfunction of synaptic neurotransmission, and further cause depressive-like behavior. The antidepressant effect of resveratrol had been widely demonstrated in previous studies; however, the underlying mechanism remains poorly understood.

Depressive-like behaviors are induced by chronic liver injury in male and female mice.

Depression is a highly prevalent mental disease and increasingly become a global public health problem. Recent studies have shown that the dysfunction of liver was associated with depression. However, the previous studies have not been fully explained the relationship between depression and liver injury.

Transcriptomic analysis reveals the mechanism of sulfasalazine-induced liver injury in mice.

Liver injury is one of the main toxic effect of sulfasalazine (SASP). However, the toxicological mechanism of SASP-induced liver injury remains unclear. In the present study, the liver injury was induced by orally treatment with SASP for 4 weeks in mice.