Aluminum Induces Neurotoxicity through the MicroRNA-98-5p/Insulin-like Growth Factor 2 Axis.

Aluminum is a well-known and widely distributed environmental neurotoxin. This study aimed to investigate the effect of miR-98-5p targeting insulin-like growth factor 2 (IGF2) on aluminum neurotoxicity. Thirty-two Sprague-Dawley rats were randomly divided into four groups and administered 0, 10, 20, and 40 μmol/kg maltol aluminum [Al(mal)], respectively.

Integrating network pharmacology and transcriptomics to study the potential mechanism of Jingzhi Niuhuang Jiedu tablet in rats with accumulation of heat in the lungs and stomach.

Ethnopharmacological Relevance: Accumulation of heat in the lungs and stomach (AHLS) is an important syndrome within the realm of traditional Chinese medicine (TCM). It is the fundamental reason behind numerous illnesses, including mouth ulcers, dermatological conditions, acne, and pharyngitis. Jingzhi Niuhuang Jiedu tablet (JN) serves as the representative prescription for treatment of AHLS clinically.

The mechanism of miR-665 targeting GNB3 in aluminum-induced neuronal apoptosis.

Background: Aluminum exerts neurotoxic effects through various mechanisms, mainly manifested as impaired learning and memory function.

Methods: Forty SD rats were divided into 0, 10, 20, and 40 mM maltol aluminum [Al(mal)] groups. Cell experiments are divided into 0, 100, 200, and 400 μM Al(mal) dose group and control, Al(mal), Al(mal)+inhibitor NC, Al(mal)+miR-665 inhibitor intervention group.

Liraglutide improved the cognitive function of diabetic mice via the receptor of advanced glycation end products down-regulation.

Background and aims Advanced glycation end products (AGEs) and receptor of advanced glycation end products (RAGE), are associated with cognition decline. We aim to investigate the effect of liraglutide on cognitive function in diabetic mice. Results Diabetic mice showed decreased cognitive function.

Ginsenoside Rb1 Alleviated High-Fat-Diet-Induced Hepatocytic Apoptosis via Peroxisome Proliferator-Activated Receptor .

Objective: High-fat-diet- (HFD-) induced hepatic cell apoptosis is common in mice with nonalcoholic fatty liver disease (NAFLD). We aim to investigate the effect of Ginsenoside Rb1 (GRb1) on hepatocyte apoptosis.

Methods: C57BL/6J mice with HFD were used to induce a liver-injured model with cell apoptosis.

Ginsenoside Rb1 increases insulin sensitivity through suppressing 11β-hydroxysteroid dehydrogenase type I.

Ginsenoside Rb1 (GRb1) is a major component of ginseng, which has been shown to ameliorate hyperglycemia in rodents and in humans with undetermined mechanisms. Here, we analyzed the molecular mechanisms by which GRb1 reduces the insulin resistance in high-fat diet (HFD)-induced mouse model for type 2 diabetes (T2D). HFD was applied for 4 weeks to induce T2D in mice, after which GRb1 was administrated and the effects on the fasting blood glucose, glucose tolerance and insulin sensitivity were analyzed.