急性肝损伤（ALI）对我们的生命构成严重威胁，已成为世界范围内的公共卫生问题。 β-胡萝卜素具有多种药理作用，例如抗炎、抗氧化和抗肿瘤活性。在本研究中，我们重点研究β-胡萝卜素对D-半乳糖胺（D-GalN）和脂多糖（LPS）诱导的ALI的保护作用和潜在分子机制。我们的结果表明，β-胡萝卜素预处理有效阻止了 LPS/D-GalN 诱导的肝脏组织病理学异常变化。同时，β-胡萝卜素预处理降低了血清丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）水平。 β-胡萝卜素预处理还降低了肝组织中丙二醛含量和髓过氧化物酶活性，增加了谷胱甘肽过氧化物酶和超氧化物歧化酶水平，并降低了肝组织中肿瘤坏死因子-a（TNF-α）和白细胞介素6（IL-6）的水平。进一步研究发现，β-胡萝卜素在LPS/D-GalN诱导的ALI中介导多种信号通路，抑制NF-κB和MAPK信号传导并上调Nrf2和HO-1蛋白的表达。所有研究结果表明，β-胡萝卜素似乎可以通过减少氧化应激和炎症（可能通过调节 NF-κB、MAPK 和 Nrf2 信号传导）来保护小鼠免受 LPS/D-GalN 诱导的 ALI。

Acute liver injury (ALI), posing a serious threaten to our life, has emerged as a public health issue around the world. β-carotene has plenty of pharmacologic effects, such as anti-inflammatory, antioxidant, and antitumor activities. In this study, we focused on studying the protective role and potential molecular mechanisms of β-carotene against D-galactosamine (D-GalN) and lipopolysaccharide (LPS) induced ALI. Our results indicated that β-carotene pretreatment effectively hindered abnormal changes induced by LPS/D-GalN in liver histopathology. Meanwhile, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were downgraded with β-carotene pretreatment. β-carotene pretreatment also decreased malondialdehyde content and myeloperoxidase activity, increased glutathione peroxidase and superoxide dismutase levels, and reduced the levels of tumor necrosis factor-a (TNF-α) and interleukin 6 (IL-6) in liver tissues. Further investigations found that β-carotene mediated multiple signaling pathways in LPS/D-GalN-induced ALI, inhibiting NF-κB and MAPK signaling and upregulating the expression of Nrf2 and HO-1 proteins. All findings indicate that β-carotene appears to protect mice against LPS/D-GalN induced ALI by reducing oxidative stress and inflammation, possibly via regulating NF-κB, MAPK, and Nrf2 signaling.