Molecular nutrition & food research · 2023
Hepatoenteric Protective Effect of Melanin from Inonotus hispidus on Acute Alcoholic Liver Injury in Mice.
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Yuan Yuan, Wu Fuquan, Zhang Fengpei, Li Xiaomin, Wu Xiaoping, Fu Junsheng
Аннотация
SCOPE: Alcoholic liver disease (ALD) is a common disease with a high incidence. Because traditional drugs have obvious side effects, it is desired to find more effective drugs.
METHODS AND RESULTS: This study investigates the effects of melanin from Inonotus hispidus fruiting bodies (IHFM) on acute alcoholic injury mice and detects the protective mechanisms via the gut-microbiota-liver axis. The results show that IHFM alleviates mouse liver injury by enhancing alcohol metabolism capacity, reducing inflammation response level and strengthening antioxidant activities. IHFM also improves mouse liver injury by activating Nrf2 signaling pathway and inhibiting toll-like receptor4 (TLR4)/nuclear factor-κβ (NF-κβ) signaling pathway. Furthermore, 16S amplification sequencing shows that IHFM can significantly increase the relative abundance of Lactobacillus reuteri and Lactobacillus johnsonii. The relative abundance of L. reuteri positively correlates with an antioxidant index, while negatively correlates with inflammatory factors.
CONCLUSION: IHFM can protect mice from acute alcoholic liver injury by upregulating the Nrf2 signaling pathway, downregulating the TLR4/NF-κβ signaling pathway, and upregulating the relative abundance of L. reuteri and L. johnsonii, representing a step forward in the development of IHFM.
METHODS AND RESULTS: This study investigates the effects of melanin from Inonotus hispidus fruiting bodies (IHFM) on acute alcoholic injury mice and detects the protective mechanisms via the gut-microbiota-liver axis. The results show that IHFM alleviates mouse liver injury by enhancing alcohol metabolism capacity, reducing inflammation response level and strengthening antioxidant activities. IHFM also improves mouse liver injury by activating Nrf2 signaling pathway and inhibiting toll-like receptor4 (TLR4)/nuclear factor-κβ (NF-κβ) signaling pathway. Furthermore, 16S amplification sequencing shows that IHFM can significantly increase the relative abundance of Lactobacillus reuteri and Lactobacillus johnsonii. The relative abundance of L. reuteri positively correlates with an antioxidant index, while negatively correlates with inflammatory factors.
CONCLUSION: IHFM can protect mice from acute alcoholic liver injury by upregulating the Nrf2 signaling pathway, downregulating the TLR4/NF-κβ signaling pathway, and upregulating the relative abundance of L. reuteri and L. johnsonii, representing a step forward in the development of IHFM.