Gut microbiota mediates methamphetamine-induced hepatic inflammation via the impairment of bile acid homeostasis

Zhang, Kaikai; Liu, Jiali; Chen, Lijian; Li, Jiahao; Yang, Jian-Zheng; Xu, Lingling; Chen, Yu-Kui; Zhang, Qin-Yao; Li, Xiuwen; Liu, Yi; Zhao, Dong; Xie, Xing; Wang, Qi

doi:10.1016/j.fct.2022.113208

Cited by 19 publications

(16 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To prepare the bacterial fluid, fecal samples from MPs or PBS-administrated mice were resuspended in sterile PBS at a concentration of 1 g/10 mL . Then, the supernatant was collected by centrifuging (900 g , 3 min, 4 °C) and immediately stored at −80 °C.…”

Section: Methodsmentioning

confidence: 99%

“…To prepare the bacterial fluid, fecal samples from MPs or PBS-administrated mice were resuspended in sterile PBS at a concentration of 1 g/10 mL. 30 Then, the supernatant was collected by centrifuging (900g, 3 min, 4 °C) and immediately stored at −80 °C. Recipient mice were pretreated with an antibiotic cocktail by oral gavage to eliminate gut microbiota (once daily, for 1 week).…”

Section: Fecal Microbial Transplant (Fmt)mentioning

confidence: 99%

“…29 Additionally, gut microbiota were reported to be involved in methamphetamine-induced hepatic inflammation by impairing the homeostasis of bile acids. 30 Concomitantly, although the disturbance of gut microbiota was also observed after MPs administration, 3 the vital role of gut microbiota in MPs-induced hepatic injuries remains unclear.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis

et al. 2023

Self Cite

View full text Add to dashboard Cite

Dietary pollution by polystyrene microplastics (MPs) can cause hepatic injuries and microbial dysbiosis. Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, exerts beneficial effects on the liver by modulating the gut microbiota. However, the role of microbiota in MPs-induced hepatic injuries and the protective effect of EGCG have not been clarified. Here, 5 μm MPs were orally administered to mice to induce hepatic injuries. Subsequently, antibiotic cocktail (ABX) and fecal microbial transplant (FMT) experiments were performed to investigate the underlying microbial mechanisms. Additionally, EGCG was orally administered to mice to explore its protection against MPs-induced hepatic injuries. Our results showed that MPs activated systemic and hepatic inflammation, promoted fibrosis, and altered the liver metabolome; meanwhile, MPs damaged the gut homeostasis by disturbing the gut microbiome, promoting colonic inflammation, and impairing the intestinal barrier. Notably, MPs reduced the abundance of the probiotics Akkermansia, Mucispirillum, and Faecalibaculum while increasing the pathogenic Tuzzerella. Interestingly, the elimination of gut microbiota mitigated MPs-induced colonic inflammation and intestinal barrier impairment. Moreover, ABX ameliorated MPs-induced systemic and hepatic inflammation but not fibrosis. Correspondingly, microbiota from MPs-administered mice induced colonic, systemic, and hepatic inflammation, while their profibrosis effect on the liver was not observed. Finally, EGCG elevated the abundance of probiotics and effectively repressed MPs-induced colonic inflammation. MPs-induced systemic and hepatic inflammation, fibrosis, and remodeling of the liver metabolome were also attenuated by EGCG. These findings illustrated that gut microbiota contributed to MPs-induced colonic and hepatic injuries, while EGCG could serve as a potential prevention strategy for these adverse consequences.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Fecal Microbial Transplant (Fmt)mentioning

confidence: 99%

See 1 more Smart Citation

Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis

et al. 2023

Self Cite

View full text Add to dashboard Cite

show abstract

“…A flowchart of the modeling process is shown in Figure 2A . Fecal microbiota transplantation (FMT) was performed as previously described ( Zhang et al, 2022b ). Feces from WT and Sig-1R knockout mice were diluted with germ-free PBS at a ratio of 1 mg/10 μL and centrifuged (4,000 × g , 10 min) to separate the supernatant.…”

Section: Methodsmentioning

confidence: 99%

Gut microbiota from sigma-1 receptor knockout mice induces depression-like behaviors and modulates the cAMP/CREB/BDNF signaling pathway

Liu

et al. 2023

Front. Microbiol.

Self Cite

View full text Add to dashboard Cite

IntroductionDepression is a common mental disorder that affects approximately 350 million people worldwide. Much remains unknown about the molecular mechanisms underlying this complex disorder. Sigma-1 receptor (Sig-1R) is expressed at high levels in the central nervous system. Increasing evidence has demonstrated a close association between the Sig-1R and depression. Recently, research has suggested that the gut microbiota may play a crucial role in the development of depression.MethodsMale Sig-1R knockout (Sig-1R KO) and wild-type (WT) mice were used for this study. All transgenic mice were of a pure C57BL/6J background. Mice received a daily gavage of vancomycin (100 mg/kg), neomycin sulfate (200 mg/kg), metronidazole (200 mg/kg), and ampicillin (200 mg/kg) for one week to deplete gut microbiota. Fecal microbiota transplantation (FMT) was conducted to assess the effects of gut microbiota. Depression-like behaviors was evaluated by tail suspension test (TST), forced swimming test (FST) and sucrose preference test (SPT). Gut microbiota was analyzed by 16s rRNA and hippocampal transcriptome changes were assessed by RNA-seq.ResultsWe found that Sig-1R knockout induced depression-like behaviors in mice, including a significant reduction in immobility time and an increase in latency to immobility in the FST and TST, which was reversed upon clearance of gut microbiota with antibiotic treatment. Sig-1R knockout significantly altered the composition of the gut microbiota. At the genus level, the abundance of Alistipes, Alloprevotella, and Lleibacterium decreased significantly. Gut microbiota dysfunction and depression-like phenotypes in Sig-1R knockout mice could be reproduced through FMT experiments. Additionally, hippocampal RNA sequencing identified multiple KEGG pathways that are associated with depression. We also discovered that the cAMP/CREB/BDNF signaling pathway is inhibited in the Sig-1R KO group along with lower expression of neurotrophic factors including CTNF, TGF-α and NGF. Fecal bacteria transplantation from Sig-1R KO mice also inhibited cAMP/CREB/BDNF signaling pathway.DiscussionIn our study, we found that the gut-brain axis may be a potential mechanism through which Sig-1R regulates depression-like behaviors. Our study provides new insights into the mechanisms by which Sig-1R regulates depression and further supports the concept of the gut-brain axis.

show abstract

“…In addition to neurotoxicity, METH can lead to hepatotoxicity, aortic aneurysm, renal dysfunction, etc. ( Ding et al, 2022 ; Luo et al, 2022 ; Zhang et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

Low and high dose methamphetamine differentially regulate synaptic structural plasticity in cortex and hippocampus

Ding

Huang²,

Xiang³

et al. 2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Psychostimulants, such as methamphetamine (METH) can induce structural remodeling of synapses by remodeling presynaptic and postsynaptic morphology. Escalating or long-lasting high dose METH accounts for neurodegeneration by targeting multiple neurotransmitters. However, the effects of low dose METH on synaptic structure and the modulation mechanism remain elusive. This study aims to assess the effects of low dose (2 mg/kg) and high dose (10 mg/kg) of METH on synaptic structure alternation in hippocampus and prefrontal cortex (PFC) and to reveal the underlying mechanism involved in the process. Low dose METH promoted spine formation, synaptic number increase, post-synaptic density length elongation, and memory function. High dose of METH induced synaptic degeneration, neuronal number loss and memory impairment. Moreover, high dose, but not low dose, of METH caused gliosis in PFC and hippocampus. Mechanism-wise, low dose METH inactivated ras-related C3 botulinum toxin substrate 1 (Rac1) and activated cell division control protein 42 homolog (Cdc42); whereas high dose METH inactivated Cdc42 and activated Rac1. We provided evidence that low and high doses of METH differentially regulate synaptic plasticity in cortex and hippocampus.

show abstract

Gut microbiota mediates methamphetamine-induced hepatic inflammation via the impairment of bile acid homeostasis

Cited by 19 publications

References 57 publications

Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis

Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis

Gut microbiota from sigma-1 receptor knockout mice induces depression-like behaviors and modulates the cAMP/CREB/BDNF signaling pathway

Low and high dose methamphetamine differentially regulate synaptic structural plasticity in cortex and hippocampus

Contact Info

Product

Resources

About