High fat diet enhances catalase loading into adipose tissue derived extracellular vesicles with limited effect on oxidative stress.

Obesity is closely related to liver disease. However, few studies have focused on the impact of adipose tissue-derived extracellular vesicles (EVs) in obesity on liver disease. Therefore, we aimed to investigate the effect of adipose tissue-derived EVs from high-fat diet (HFD)-fed obese mice (EV-HFD) on liver damage induced by oxidative stress.

Ginsenoside Rh2 Mitigates Endoplasmic Reticulum Stress-Induced Apoptosis and Inflammation and Through Inhibition of Hepatocyte-Macrophage Inflammatory Crosstalk.

Endoplasmic reticulum stress (ERS) contributes to hepatocyte inflammation, triggered by prolonged exposure to lipotoxicity, and promotes non-alcoholic fatty liver disease (NAFLD) progression by recruiting and activating hepatic macrophages, which accelerate fibrosis and exacerbate disease progression. Here, we aimed to evaluate the therapeutic potential of ginsenoside Rh2 (Rh2) in a cell model of NAFLD induced by the ERS inducer thapsigargin (THA). HepG2 cells were treated with THA to induce ERS and mimic NAFLD conditions.

Salmon Nasal Cartilage-Derived Proteoglycans Alleviate Monosodium Iodoacetate-Induced Osteoarthritis in Rats.

Osteoarthritis is a chronic inflammatory condition characterized by the degeneration of joint cartilage and underlying bone, resulting in pain, swelling, and reduced mobility. This study evaluates the efficacy of salmon nasal cartilage-derived proteoglycans in mitigating osteoarthritis symptoms and investigates the underlying molecular mechanisms. This study employed a rat model of osteoarthritis induced by monosodium iodoacetate (MIA) injection.

Adipose tissue-derived extracellular vesicles from obese mice suppressed splenocyte-mediated pancreatic cancer cell death.

Background: Obesity is a risk factor for pancreatic cancer and negatively contributes to the immune system. However, the mechanisms by which obesity mediates these actions are still poorly understood. Recent studies have demonstrated that extracellular vesicles (EVs) are key mediators of communication between cells and may influence various aspects of cancer progression.

Adipose tissue-derived exosomes contribute to obesity-associated liver diseases in long-term high-fat diet-fed mice, but not in short-term.

Introduction: Our study aimed to investigate the changes in hepatic endoplasmic reticulum (ER) stress, inflammation, insulin signaling, and lipid metabolism during the administration of a high-fat diet (HFD) in mice in order to identify correlations between obesity and metabolic disease development in the liver.

Methods: We used short-, medium-, and long-term HFD periods, corresponding to 4, 8, and 12 weeks, respectively, and isolated exosomes from adipose tissue. We confirmed the effect of adipose tissue-derived exosomes on metabolic disorders in obesity in alpha mouse liver 12 (AML12) hepatocytes.

Liver-Derived Exosomes Induce Inflammation and Lipogenesis in Mice Fed High-Energy Diets.

The liver is an endocrine organ and is the first organ exposed to nutrients when they are absorbed into the body before being metabolized by the distal organs. Although the liver plays an essential role in the interactions between the metabolic organs, their regulatory mechanisms have not been elucidated. Exosomes mediate communication between cells and primarily enable the transport of lipids, mRNAs, miRNAs, and proteins between cells.

Overcoming the Intrinsic Gefitinib-resistance via Downregulation of AXL in Non-small Cell Lung Cancer.

Background: Resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib, is a limited factor in the treatment of non-small-cell lung cancer (NSCLC) patients. Therefore, ongoing studies are trying to identify EGFR-TKIs-resistant mechanisms and to discover novel therapeutic strategies and targets for NSCLC treatment.

Methods: In the present study, the possibility of overcoming intrinsic gefitinib-resistance was examined by regulating the expression of AXL.