[en] Highlights: • AgI nanoparticle/BiOI nanosheet composites were successfully fabricated via the hydrothermal method of precipitation and the ion-exchange method. • The kinetic photocatalytic degradation was controlled by a pseudo-first-order kinetic model. • Visible-light-driven photocatalytic performance of composites was enhanced and optimized by adjusting the component ratio. • Under Xe lamp irradation as visible light source, the 50% AgI NP/BiOI NS composite showed the highest photocatalytic activity in the degradation of MO and CBB dye in water. Nanosheet BiOI materials were synthesized using the precipitation-hydrothermal method. Subsequently, nanoparticle AgI/BiOI nanosheet composites were fabricated using an ion-exchange method and a controlled amount of BiOI. The phase composition, optical morphology, and absorption properties of the samples were determined using XRD, SEM, XPS, TEM, HRTEM, BET, and UV–Vis diffuse reflectance. Organic dyes, such as methyl orange (MO) and Coomassie brilliant blue R-250 (CBB), were used to check the composites’ photocatalytic performance undergoing photodegradation in visible light. The prepared composites had high purity, and the AgI nanoparticles were evenly loaded on the flower-like BiOI nanosheets, both absorbing the visible light. The 50% AgI NP/BiOI NS compound demonstrated the best visible photocatalytic activity and degraded rate of 96.9% and 97% of the MO and CBB dye, respectively, under visible light for 30​min. The photocatalytic activity of sole BiOI or AgI was poor, whereas the composites were much better. The composite with 50% AgI exhibited the best photocatalytic activity because of the formation of a heterojunction, which promotes the separation of photogenerated carriers, making AgI stable under visible-light irradiation.

[en] Acute liver injury (ALI) is characteristic of abrupt hepatic dysfunction and inflammatory response. Activaion of Kupffer cells (KCs) plays a central role in the pathogenesis of ALI. Since the High Mobility Group A protein2 (HMGA2) occurs as a driver at critical stage of hepatocellular carcinoma, herein, we investigated the role of HMGA2 in macrophage activation during ALI. Our study found that the expression of HMGA2 decreased dramatically both in KCs isolated from the liver in mice with ALI and in LPS-induced RAW264.7 cell lines. Moreover, loss- and gain-of-function studies suggested that HMGA2 could enhance the expression of pro-inflammatory cytokines including TNF-α, IL-6 and IL-1β. These results indicated that HMGA2 may play an essential role in macrophage activation during ALI. Additionally, our results showed the expression of HMGA2 was up-regulated when LPS-induced RAW264.7 cells were treated with 5-aza-2-deoxycytidine. Furthermore, silencing of DNMT1, DNMT3a, DNMT3b could respectively prevent the down-expression of HMGA2 in LPS-induced RAW264.7 cells. In conclusion, HMGA2 promotes the release of pro-inflammatory cytokines through NF-κB pathway, and the dysregulation of HMGA2 may involve with hypermethylation. - Highlights: • HMGA2 was screened through RRBS by our research group. • Our study provides the first evidence to demonstrated the function of HMGA2 in acute liver injury. • HMGA2 mediated inflammation is associated with hypermethylation was illustrated for the first time.