Formula alleviates diabetic podocyte injury by regulating miR-21a-5p/FoxO1/PINK1-mediated mitochondrial autophagy.

Objectives: To investigate the protective effect of Formula (YYHT) against high glucose-induced injury in mouse renal podocytes (MPC5 cells) and the possible mechanism.

Methods: Adult Wistar rats were treated with 19, 38, and 76 g/kg YYHT or saline via gavage for 7 days to prepare YYHT-medicated or blank sera for treatment of MPC5 cells cultured in high glucose (30 mmol/L) prior to transfection with a miR-21a-5p inhibitor or a miR-21a-5p mimic. The changes in miR-21a-5p expressions and the mRNA levels of FoxO1, PINK1, and Parkin in the treated cells were detected with qRT-PCR, and the protein levels of nephrin, podocin, FoxO1, PINK1, and Parkin were detected with Western blotting.

Development and experimental validation of a senescence-related long non-coding RNA signature for prognostic prediction and immune microenvironment characterization in gastric cancer patients.

Background: Cellular senescence is considered a new marker of cancer. It has been suggested that long non-coding RNA (lncRNA) can be used to predict the prognosis of cancers. However, it remains to be seen whether the lncRNAs associated with cellular senescence can be used to predict the prognosis of gastric cancer (GC).

Establishment and application of a sandwich ELISA method for measuring Toxoplasma gondii circulating fructose-1,6-bisphosphate aldolase (ALD) protein in cats.

Toxoplasmosis is an important public health concern. Cats play a crucial role in increasing the risk of toxoplasmosis transmission to humans. Early diagnosis in cats is essential for the prevention and control of toxoplasmosis.

Methamphetamine inhibits huntingtin-associated protein 1-mediated tyrosine receptor kinase B endocytosis resulting the neuroprotective dysfunction of brain-derived neurotrophic factor.

Methamphetamine (METH), a synthetic stimulant, has seen an escalating abuse situation globally over the past decade. Although the molecular mechanism underlying METH-induced neurotoxicity has been explored, the dysfunction of brain-derived neurotrophic factor (BDNF) neuroprotection in the context of METH neurotoxicity remains insufficiently understood. Our previous studies have found that METH induced neurotoxicity and BDNF expression in rat primary neurons, necessitating further research into this paradox.