Pharmacological Effects of Urolithin A and Its Role in Muscle Health and Performance: Current Knowledge and Prospects.

Urolithin A (UA) is a naturally occurring compound derived from the metabolism of gut microbiota, which has attracted considerable research attention due to its pharmacological effects and potential implications in muscle health and performance. Recent studies have demonstrated that Urolithin A exhibits diverse biological activities, encompassing anti-inflammatory, antioxidant, anti-tumor, and anti-aging properties. In terms of muscle health, accumulating evidence suggests that Urolithin A may promote muscle protein synthesis and muscle growth through various pathways, offering promise in mitigating muscle atrophy. Moreover, Urolithin A exhibits the potential to enhance muscle health and performance by improving mitochondrial function and regulating autophagy. Nonetheless, further comprehensive investigations are still warranted to elucidate the underlying mechanisms of Urolithin A and to assess its feasibility and safety in human subjects, thereby advancing its potential applications in the realms of muscle health and performance.

Presence of different microplastics promotes greenhouse gas emissions and alters the microbial community composition of farmland soil.

Microplastics (MPs) are regarded as potential persistent organic pollutants owing to their small size and low degradability. However, the effect of MP pollution on greenhouse gas (GHG) emissions from farmland soil is yet unclear. Therefore, a series of microcosm experiments were set up using polyvinyl chloride (PVC), polypropylene (PP), polyethylene (PE), polystyrene (PS), and polyester (PET) at concentrations of 0.25 %, 2 %, and 7 % (w/w). Each treatment had three replicates. This experiment was carried out to verify the effect of MP pollution on greenhouse gas (GHG) emissions from farmland soil. The results showed that the addition of MPs significantly promoted the emissions of the three main GHGs, including nitrous oxide (N2O), carbon dioxide (CO2), and methane (CH4). Especially, PE may cause most GHG emissions which would contribute to climate warming when its pollution concentration increased. In addition, different doses and types of MPs could affect microbial community structure. These findings of this present study may provide a scientific and practical reference for the prevention and control of MPs pollution and risk assessment of global climate change caused by MPs.

Physiological response and oxidative stress of grass carp (Ctenopharyngodon idellus) under single and combined toxicity of polystyrene microplastics and cadmium.

The harm of microplastics (MPs) to aquatic ecosystems is caused by their stable and non-degradable properties. Additionally, the pollutants such as heavy metals in the water are easy to be adsorbed on their surface with their small particle size and large specific surface area, resulting in environmental pollution. Therefore, the study on the mixture toxicity of MPs and heavy metals has theoretical significance for the risk assessment of aquatic ecosystems. In the present study, 10 nm polystyrene (PS) and cadmium (Cd) were used, and their individual and mixture acute toxicities on grass carp (Ctenopharyngodon idellus) were examined. The results indicated that the mortality of the fish increased with the concentration from 10 mg L-1 to 20 mg L-1, and the existence of PS-MPs elevated the Cd concentrations in the fish and accelerated the death. Whether the Cd and/or the PS-MPs concentrations caused varying degrees of damage to the gills, kidney, liver, and muscles of the grass carp, especially under the highest concentrations (20 mg L-1 Cd + 300 µg L-1 PS-MPs). Moreover, low concentrations of PS-MPs alone (30 µg L-1 PS-MPs) significantly increased the superoxide dismutase (SOD) activity in the kidney and liver, reaching 12.43% and 14.38%, respectively (P < 0.05). The peroxidase (POD) activity was increased only in the kidney, up to 25.95% (P < 0.05). Also, significant reductions in SOD and POD activities were observed in the combination of high concentration of Cd (20 mg L-1) and 300 µg L-1 PS-MPs (P < 0.05). To the best of our knowledge, there are few studies on the impact of combined toxicity of PS-MPs and Cd on grass carp under laboratory conditions. Therefore, these findings may provide a theoretical guarantee for pollution prevention and control in the aquatic ecosystem.

LncRNA SNHG12 promotes the malignant progression of melanoma by targeting miR-199b.

Background: Melanoma is a type of tumor caused by the malignant transformation of melanocytes, and has a high degree of malignancy. Small nucleolar RNA host gene 12 (SNHG12) plays an important role in a variety of cancers, but its role in melanoma and its mechanisms are still unclear. In this study, we measured the expression of SNHG12 and explored the molecular mechanisms involved in melanoma. Methods: We detected the expression level of SNHG12 in melanoma cell lines, and explored the effect of SNHG12 on the proliferation, migration, and invasion of melanoma cells in vitro. Mechanistic studies explored the regulation of downstream genes by SNHG12. Results: Overexpression of SNHG12 was found in melanoma cell lines, and SNHG12 promoted the proliferation, migration, and invasion of melanoma cells. MiR-199b is a target gene of SNHG12, which was expressed at low levels in melanoma cell lines, and SNHG12 regulated melanoma cell proliferation, migration, and invasion through miR-199b. We also revealed that SNHG12 promoted the expression of the target genes of miR-199b, namely ETS1, PXN, JAG1, and DDR1. Conclusions: SNHG12 is highly expressed in melanoma, and promotes the expression of ETS1, PXN, JAG1, and DDR1 through targeted regulation of miR-199b, thereby promoting the proliferation, migration, and invasion of melanoma cells.

Dioscin induces ferroptosis and synergistic cytotoxicity with chemotherapeutics in melanoma cells.

In this study, we evaluated the anti-tumor effects of dioscin, a steroidal saponin, on melanoma cells. Dioscin significantly inhibited cell viability and induced cell death of melanoma cells in a time- and dose- dependent manner. Furthermore, dioscin increased the concentration of intracellular ferrous irons, MDA and ROS. This effect could be inhibited by L-g-glutamyl-p-nitroanilide (GPNA), compound 968 and ferroptosis inhibitor ferrostatin-1 (Fer-1). Furthermore, dioscin induced ferroptosis by affecting the expression of transferrin and ferroportin which are regulators of intracellular levels of iron. Finally, dioscin in combination with various chemotherapeutic agents showed synergistic effects against melanoma cells. Our data suggested that dioscin exerted anti-tumor effects in melanoma cells by inducing ferroptosis. Dioscin alone or with other agents might be applied as a promising strategy to treat melanoma.

miR-495 inhibits proliferation, migration, and invasion and induces apoptosis via inhibiting PBX3 in melanoma cells.

BACKGROUND: Amounting evidence indicate that miRNAs play an important role in the development of various cancers. MiR-495 is a potential tumor suppressor in cancers, however its role in melanoma is still elusive. The study aimed to investigate the role of miR-495 and the underlying mechanisms in melanoma cells. METHODS: The levels of miR-495 in melanoma tissues and cell lines were measured by quantitative real-time polymerase chain reaction. Mimics of miR-495 was transfected into human melanoma cells A375 and MeWo. Cell viability of miR-495-transfected cells was assayed by MTT assay. Cell migration and invasion of miR-495 transfected cells were measured by wound healing assay and transwell assay, respectively. Nucleosome enzyme-linked immunosorbent assay was performed to measure the apoptosis induced by overexpression of miR-495. Luciferase reporter assays were performed to verify the interaction between miR-495 and its target PBX3. RESULTS: It was found that the expression levels of miR-495 were down-regulated in melanoma tissues and cells. Moreover, overexpression of miR-495 inhibited melanoma cell proliferation, migration and invasion in vitro. PBX3 was identified as a target for inhibition by miR-495 and was confirmed by luciferase assay, quantitative real-time polymerase chain reaction and western blot. We also indicated that silencing of PBX3 also repressed melanoma cell proliferation, migration and invasion in vitro. CONCLUSION: In summary, our findings demonstrated that miR-495 functions as a tumor suppressor in human melanoma via directly targeting PBX3.