polysaccharide boosts osteogenic differentiation of bone marrow mesenchymal stem cells by Wnt/β-catenin signaling.

Objectives: To investigate the role of Morinda officinalis polysaccharide (MOP) in the protein expression of the Wnt/β-catenin signaling cascade during the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), and to elucidate the mechanisms by which MOP enhances osteogenic differentiation at the cellular level.

Methods: BMSCs were isolated and cultured using the whole bone marrow adherence method, followed by flow cytometry for the detection of BMSC marker antigens. Two groups were prepared: a low-dose MOP (L-MOP, 10 µg/mL) group and a high-dose MOP (H-MOP, 40 µg/mL) group.

Curcumin attenuates aflatoxin B1-induced ileum injury in ducks by inhibiting NLRP3 inflammasome and regulating TLR4/NF-κB signaling pathway.

Aflatoxin B1 (AFB1) is a widespread toxic contamination in feed for animals. The primary active component of turmeric, curcumin (Cur), is an antioxidant and an anti-inflammatory. However, it is yet unknown how AFB1 affects the intestinal epithelial barrier and whether Cur acts as a protective mechanism when exposed to AFB1.

Arsenic-Induced Ferroptosis in Chicken Hepatocytes via the Mitochondrial ROS Pathway.

Arsenic has been shown to be highly toxic and can cause liver damage. Previous studies have shown that arsenic causes severe liver damage and induces accumulation of reactive oxygen species (ROS). This study aimed to investigate the effects of ferroptosis on the liver in arsenic trioxide (ATO) and to explore the underlying mechanisms.

Multi-omics reveals the protective effects of curcumin against AFB1-induced oxidative stress and inflammatory damage in duckling intestines.

Aflatoxin B1 (AFB1) is the most prevalent and toxic class of aflatoxins, which is considered a significant risk factor for food safety. Curcumin, a phytoconstituent with anti-inflammatory and antioxidant properties, has potential therapeutic value for intestinal inflammatory diseases. In this study, the duckling model susceptible to AFB1 was selected for toxicity testing, aiming to explore the effect of curcumin on AFB1 enterotoxicity and its possible mechanism of action.

Arsenic induced neurotoxicity in the brain of ducks: The potential involvement of the gut-brain axis.

Background: Arsenic is a widely distributed ecotoxic pollutant that has been found to cause neurotoxicity in a variety of species. Gut-brain axis is a two-way information network between the gut microbiome and the brain, which is closely related to organismal health. However, the role of the gut-brain axis in arsenic-induced neurotoxicity remains largely unknown.

Curcumin alleviates AFB1-induced nephrotoxicity in ducks: regulating mitochondrial oxidative stress, ferritinophagy, and ferroptosis.

Aflatoxin B1 (AFB1), an extremely toxic mycotoxin that extensively contaminates feed and food worldwide, poses a major hazard to poultry and human health. Curcumin, a polyphenol derived from turmeric, has attracted great attention due to its wonderful antioxidant properties. Nevertheless, effects of curcumin on the kidneys of ducks exposed to AFB1 remain unclear.

Curcumin attenuates AFB1-induced duck liver injury by inhibiting oxidative stress and lysosomal damage.

Aflatoxin B1 (AFB1), as the most toxic secondary metabolite produced by Aspergillus flavus, is a serious threat to human and animal health. Curcumin, a polyphenol from the plant turmeric, has demonstrated unique anti-damage properties in several studies. But, its ability to alleviate AFB1-induced liver damage in ducks and the underlying mechanisms are not completely elucidated.

Combined effect of arsenic and polystyrene-nanoplastics at environmentally relevant concentrations in mice liver: Activation of apoptosis, pyroptosis and excessive autophagy.

The ecological risks caused by the coexistence of pollutants such as arsenic (As) and polystyrene-nanoplastics (PSNPs) in the environment have become a non-negligible problem. However, the effects of As and PSNPs co-exposure on mammals and the underlying toxicity mechanisms have remained unclear. Therefore, the present study established mouse models of As and/or PSNPS exposure to systematically analyze the underlying role of autophagy, apoptosis and pyroptosis in hepatotoxicity induced by co-exposure of As and PSNPs.

Curcumin activates the Nrf2 Pathway to alleviate AFB1-induced immunosuppression in the spleen of ducklings.

Ducklings is one of the most susceptible poultry to Aflatoxin B1 (AFB1) which widely existed in duckling products will also in turn affect human health. Curcumin (CUR) has significant effects on immune regulation and anti-oxidation. But whether CUR alleviates toxic effects on duckling spleen induced by AFB1 remains largely unknown.

Shikonin-mediated PD-L1 degradation suppresses immune evasion in pancreatic cancer by inhibiting NF-κB/STAT3 and NF-κB/CSN5 signaling pathways.

Background: Pancreatic cancer (PC) is a highly fatal malignancy with few effective therapies currently available. Recent studies have shown that PD-L1 inhibitors could be potential therapeutic targets for the treatment of PC. The present study aims to investigate the effect of Shikonin on immune evasion in PC with the involvement of the PD-L1 degradation.

Overexpression of long non-coding RNA00355 enhances proliferation, chemotaxis, and metastasis in colon cancer via promoting GTF2B-mediated ITGA2.

Long non-coding RNAs (LncRNAs) can regulate physiological and pathological functions, exhibiting a wide range of roles in cell biology. Moreover, many lncRNAs are dysregulated in various cancers, including colon cancer. In this study, we investigated the role of the lncRNA LINC00355 in colon cancer, after first establishing its interaction with GTF2B, and ITGA2 on the LncMap database.

Downregulation of long non-coding RNA MAFG-AS1 represses tumorigenesis of colorectal cancer cells through the microRNA-149-3p-dependent inhibition of HOXB8.

Background: Colorectal cancer (CRC) is considered as the second common death-induced cancer. More recently, association of long non-coding RNAs (lncRNAs) with CRC has been extensively investigated. Therefore, the present study was performed to determine whether lncRNA MAF BZIP Transcription Factor G Antisense RNA 1 (MAFG-AS1) could regulate biological activities of CRC cells and unravel the underlying mechanisms.

RETRACTED: KYA1797K down-regulates PD-L1 in colon cancer stem cells to block immune evasion by suppressing the β-catenin/STT3 signaling pathway.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).

Exogenous hydrogen sulfide protects fatty liver against ischemia-reperfusion injury by regulating endoplasmic reticulum stress-induced autophagy in macrophage through mediating the class A scavenger receptor pathway in rats.

Fatty liver disease is a disease manifested with excessive alcohol intake and obese. Importantly, hydrogen sulfide (H S) has been revealed to participate in the progression of fatty liver; however, the underlying mechanism has not been clearly elucidated yet. In this study, we aimed to investigate the effects of exogenous H S on fatty liver ischemia-reperfusion injury (IRI) through mediating class A scavenger receptor (SRA) pathway in rats.

Regulation of Long Non-Coding RNA-Dreh Involved in Proliferation and Migration of Hepatic Progenitor Cells during Liver Regeneration in Rats.

Liver regeneration plays a significant role in protecting liver function after liver injury or chronic liver disease. Long non-coding RNAs (lncRNAs) are considered to be involved in the proliferation of hepatocytes and liver regeneration. Therefore, this study aimed to explore the effects of LncRNA-Dreh on the regulation of hepatic progenitor cells (HPCs) during liver regeneration in rats.

Characterization of peripheral blood T lymphocyte subsets in Chinese rhesus macaques with repeated or long-term infection with Plasmodium cynomolgi.

T lymphocytes play a vital role in antimalaria immunity, but there is little information about the role of T cells in malaria infection. In order to explore the profile of T cells in malaria immunity, we infected Chinese rhesus macaques with the malaria parasite (Plasmodium cynomolgi) and examined the dynamics of T cell subsets. Both repeated and long-term infections were involved.