Anti-inflammatory, cardioprotective effect of gypenoside against isoproterenol-induced cardiac remodeling in rats via alteration of inflammation and gut microbiota.

Background: Myocardial infarction (MI), commonly referred to as a heart attack, occurs when the blood flow to a portion of the heart is blocked, causing damage to the heart muscle. In this study, we scrutinized the cardioprotective effect of gypenoside against the isoproterenol (ISO)-induced myocardial injury (MI) in the rats.

Methods: Wistar rats were divided into four groups as follow: normal, gypenoside (10 mg/kg), ISO control, and ISO control treated with the gypenoside (2.

Cartilage Damage Pathological Characteristics of Diabetic Neuropathic Osteoarthropathy.

Background: Diabetic neuropathic osteoarthropathy (DNOAP) is a rare and easily missed complication for diabetes that leads to increased morbidity and mortality. DNOAP is characterized by progressive destruction of bone and joint, but its pathogenesis remains elusive. We herein aimed to investigate the pathological features and pathogenesis of the cartilages damage in DNOAP patients.

piRNA-6426 increases DNMT3B-mediated SOAT1 methylation and improves heart failure.

Purpose: Previous studies found that piRNAs could participate in disease progression by regulating DNA methylation, but there are few reports on their roles in heart failure (HF).

Methods: The level of piRNA-6426 in the venous blood of HF patients and volunteers was detected by RT-qPCR. Hypoxia-induced cardiomyocytes were transfected with lentiviral-mediated piRNA-6426 overexpression vector (LV-piRNA-6426) or together with LV-DNMT3B, and then cell viability and apoptosis, glucose uptake, ROS production, LDH activity and secretion of inflammatory factors were detected.

Genetic Variants and Protein Alterations of Selenium- and T-2 Toxin-Responsive Genes Are Associated With Chondrocytic Damage in Endemic Osteoarthropathy.

The mechanism of environmental factors in Kashin-Beck disease (KBD) remains unknown. We aimed to identify single nucleotide polymorphisms (SNPs) and protein alterations of selenium- and T-2 toxin-responsive genes to provide new evidence of chondrocytic damage in KBD. This study sampled the cubital venous blood of 258 subjects including 129 sex-matched KBD patients and 129 healthy controls for SNP detection.

Role of Exosomal MicroRNAs and Their Crosstalk with Oxidative Stress in the Pathogenesis of Osteoporosis.

Osteoporosis (OP) is an aging-related disease involving permanent bone tissue atrophy. Most patients with OP show high levels of oxidative stress (OS), which destroys the microstructure of bone tissue and promotes disease progression. Exosomes (exos) help in the delivery of microRNAs (miRNAs) and allow intercellular communication.

Analysis of the association and predictive value of hyperhomocysteinaemia for obstructive coronary artery disease.

Objective: To investigate the predictive value of hyperhomocysteinaemia (HHcy) for obstructive coronary artery disease (CAD) in an Asian population in northern China.

Methods: This retrospective study enrolled patients at their first cardiac assessment and assigned them to an obstructive CAD group or a non-obstructive CAD group according to the coronary angiography results. HHcy was defined as a homocysteine (Hcy) level > 15 µmol/l.

MiR-23a Is Involved in Myocardial Ischemia/Reperfusion Injury by Directly Targeting CX43 and Regulating Mitophagy.

Activation of CX43 signaling protects myocardial cells from myocardial ischemia/reperfusion (I/R) injury. However, the underlying mechanism remains unclear. MicroRNAs (miRNAs) are well known to play important roles in the progression of diverse diseases.

Rosmarinic acid ameliorated cardiac dysfunction and mitochondrial injury in diabetic cardiomyopathy mice via activation of the SIRT1/PGC-1α pathway.

Mitochondrial injury plays an essential role in the pathogenesis of diabetic cardiomyopathy (DCM). Previous studies demonstrated that rosmarinic acid (RA) treatment prevented high glucose-induced mitochondrial injury in vitro. However, whether RA can ameliorate cardiac function by preventing mitochondrial injury in DCM is unknown.

[Rosmarinic acid inhibits high glucose-induced cardiomyocyte hypertrophy by activating Parkin-mediated mitophagy].

Objective: To evaluate the effect of rosmarinic acid (RA) on mitophagy and hypertrophy of cardiomyocytes exposed to high glucose (HG).

Methods: Rat cardiomyocytes (H9c2) exposed to HG (25 mmol/L) were treated with 50 μmol/L RA or with both RA treatment and Parkin siRNA transfection, with the cells cultured in normal glucose (5.5 mmol/L) and HG as the controls.

Protective and therapeutic effects of Trianthema portulacastrum against atherosclerosis in male albino rats via G-protein-coupled receptor 124.

Atherosclerosis is a severe cardiovascular disease characterized by narrowing of the lumen, plaque formation, and blood flow turbulence as a result of cholesterol and lipid accumulation in the inner lining of arteries. Bishkhapra (Trianthema portulacastrum Linn.) is a well-known common weed belonging to the family Aizoaceae.

Lin28a protects against diabetic cardiomyopathy through Mst1 inhibition.

Lin28a has been found to enhance glucose uptake and insulin sensitivity. Lin28a alleviates cardiac dysfunction under various pathological conditions. However, the effects and underlying mechanisms of Lin28a on diabetic cardiomyopathy (DCM) are not well-understood.

Effects of resveratrol on regulation on UCP2 and cardiac function in diabetic rats.

Mitochondrial dysfunction is essential in the development and prognosis of diabetic cardiomyopathy (DCM). Resveratrol (RES) is thought as a mitochondrial protector. In this study, we hypothesized that RES may ameliorate mitochondrial function and consequently improve cardiac function in diabetic rats, and uncoupling protein 2 (UCP2) was involved in the protective effects of RES on DCM.

Pathogenesis and potential relative risk factors of diabetic neuropathic osteoarthropathy.

Diabetic neuropathic osteoarthropathy (DNOAP) is an uncommon, but with considerable morbidity and mortality rates, complication of diabetes. The real pathogenesis is still unclear. The two popular theories are the neuro-vascular theory and neuro-traumatic theory.

Inhibition of Drp1 attenuates mitochondrial damage and myocardial injury in Coxsackievirus B3 induced myocarditis.

Viral myocarditis (VMC) is closely related to apoptosis, oxidative stress, innate immunity, and energy metabolism, which are all linked to mitochondrial dysfunction. A close nexus between mitochondrial dynamics and cardiovascular disease with mitochondrial dysfunction has been deeply researched, but there is still no relevant report in viral myocarditis. In this study, we aimed to explore the role of Dynamin-related protein 1 (Drp1)-linked mitochondrial fission in VMC.

Rosmarinic Acid suppressed high glucose-induced apoptosis in H9c2 cells by ameliorating the mitochondrial function and activating STAT3.

Mitochondrial injury characterized by intracellular reactive oxygen species (ROS) accumulation plays a critical role in hyperglycemia-induced myocardium dysfunction. Previous studies have demonstrated that Rosmarinic Acid (RA) treatment and activating Signal transducer and activator of transcription 3 (STAT3) signaling pathway have protective effects on mitochondrial dysfunction in cardiomyocyte, but there is little data regarding cardiomyocyte under condition of high-glucose. The present study was undertaken to determine the relationship between RA and STAT3 activation, as well as their effects on high glucose-induced mitochondrial injury and apoptosis in H9c2 cardiomyocyte.

Involvement of caspases and their upstream regulators in myocardial apoptosis in a rat model of selenium deficiency-induced dilated cardiomyopathy.

Keshan disease is an endemic dilated cardiomyopathy (DCM) which is closely related with selenium-deficient diet in China. In the previous study, we reported that the low selenium status plays a pivotal role in the myocardial apoptosis in the DCM rats, however, the underlying mechanism remains unclear. The present study aimed to determine whether the intrinsic, extrinsic pathways and the upstream regulators were involved in the myocardial apoptosis of selenium deficiency-induced DCM rats.