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the opposite was true for the administered group compared with the model group, suggesting that the treatment of hepatobiliary injury was achieved by regulating the abundance of the above-mentioned bacterial groups

These two major pathological hallmarks contribute to changes in numerous cellular and subcellular events, such as mitochondrial dysfunction, redox imbalance, and neuroinflammation that lead to activation of neurotoxic cascade towards cell death, thereby impairing synaptic communication [81,82]