A5013795191- Mitochondrial Function and Pathology
- Chemotherapy-induced cardiotoxicity and mitigation
- Cardiac Ischemia and Reperfusion
- Adipose Tissue and Metabolism
- Electron Spin Resonance Studies
- Nicotinic Acetylcholine Receptors Study
- Neuroinflammation and Neurodegeneration Mechanisms
- Vagus Nerve Stimulation Research
- Cardiac electrophysiology and arrhythmias
- Cancer-related cognitive impairment studies
- Heart Rate Variability and Autonomic Control
- Metabolism and Genetic Disorders
- Trace Elements in Health
- Diet and metabolism studies
- Cardiac Fibrosis and Remodeling
- Cardiovascular Function and Risk Factors
- Cardiac Imaging and Diagnostics
- Anesthesia and Neurotoxicity Research
- Ion channel regulation and function
- Metabolism, Diabetes, and Cancer
- Neurological Disease Mechanisms and Treatments
- Nitric Oxide and Endothelin Effects
- Inflammasome and immune disorders
- Tryptophan and brain disorders
- Circadian rhythm and melatonin
Chiang Mai University
2017-2025
An uncontrolled balance of mitochondrial dynamics has been shown to contribute cardiac dysfunction during ischemia/reperfusion (I/R) injury. Although inhibition fission could ameliorate dysfunction, modulation fusion by giving a promoter at different time-points I/R injury never investigated. We hypothesized that exerts cardioprotection with levels efficacy in rats Forty male Wistar were subjected 30-min ischemia coronary occlusion, followed 120-min reperfusion. The then randomly divided...
Altered cardiac mitochondrial dynamics with excessive fission is a predominant cause of dysfunction during ischemia/reperfusion (I/R) injury. Although pre-ischemic inhibition has been shown to improve function in I/R injury, the effects this inhibitor given at different time-points injury are unknown. Fifty male Wistar rats were subjected sham and For randomly divided into pre-ischemia, during-ischemia, upon onset reperfusion group. A inhibitor, Mdivi-1 (mitochondrial division 1) (1.2 mg/kg)...
Background Cardiac ischemic/reperfusion (I/R) injury leads to brain damage. A new antihyperlipidemic drug is aimed at inhibiting PCSK 9 (proprotein convertase subtilisin/kexin type 9), a molecule first identified in neuronal apoptosis paradigm. Thus, the inhibitor ( 9i) may play role recovery following cardiac I/R insults. We hypothesize that 9i attenuates damage caused by via diminishing microglial/astrocytic hyperactivation, β-amyloid aggregation, and loss of dendritic spine. Methods...
Abstract During acute cardiac ischaemia/reperfusion (I/R), an increased plasma proprotein convertase subtilisin/kexin 9 (PCSK9) level instigates inflammatory and oxidative processes within ventricular myocytes, resulting in dysfunction. Therefore, PCSK9 inhibitor (PCSK9i) might exert cardioprotection against I/R injury. However, the effects of PCSK9i on heart during injury have not been investigated. The given at different time‐points left (LV) function were Male Wistar rats subjected to...
Abstract Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized differently myocardial damage during acute I/R Rats underwent or sham operation. I/R‐operated rats were divided into 4 groups: vehicle, (Z‐vad), ferroptosis (Fer‐1) (Nec‐1) inhibition. in each inhibitor group subdivided 3 different dose regimens: low, medium high. Infarct size, left ventricular (LV)...
Abstract Background Myocardial infarction (MI) has recently accounted for more than one-third of global mortality. Multiple molecular pathological pathways, such as oxidative stress, inflammation, and mitochondrial dysfunction, have been recognized possible mechanisms in the development MI. Furthermore, different phases ischemic injury following progression MI were also associated with multiple types programmed cell death (PCDs), including apoptosis, necroptosis, ferroptosis, pyroptosis....
Abstract Obese insulin resistance impairs cardiac mitochondrial dynamics by increasing fission and decreasing fusion, leading to damage, myocardial cell death dysfunction. Therefore, inhibiting promoting fusion could provide cardioprotection in this pre-diabetic condition. We investigated the combined effects of inhibitor (Mdivi1) promoter (M1) on function obese insulin-resistant rats. hypothesized that Mdivi1 M1 protect heart against condition, but also there will be greater improvement...
Background: We have previously demonstrated that oxidative stress and brain mitochondrial dysfunction are key mediators of pathology during myocardial infarction (MI). Objective: To investigate the beneficial effects dynamic modulators, including fission inhibitor (Mdivi-1) fusion promotor (M1), on cognitive function molecular signaling in MI rats comparison with effect enalapril. Methods: Male were assigned to either sham or operation. In group, an ejection Fraction less than 50% included,...
Doxorubicin (DOX), an effective, extensively used chemotherapeutic drug, can cause cognitive deterioration in cancer patients. The associated debilitating neurological sequelae are referred to as chemobrain. Our recent work demonstrated that Dox treatment resulted imbalance mitochondrial dynamics, ultimately culminating decline rats. Therefore, this study, we aim explore the therapeutic efficacy of a pharmacological intervention, which modulates dynamics using potent fission inhibitor...
Changes in mitochondrial dynamics have been recognized as being one of the mechanisms related to cardiotoxicity following a high cumulative dose doxorubicin (DOX). A division inhibitor-1 (Mdivi-1) and fusion promoter (M1) shown be cardioprotective variety cardiovascular settings, however, their anticardiotoxic efficacy against DOX therapy remains unclear. We therefore investigated whether treatment with Mdivi-1 M1 protects heart DOX-induced via mitochondria-targeted pathways. Male Wistar...
Trastuzumab (Trz)-induced cardiotoxicity (TIC) is one of the most common adverse effects targeted anticancer agents. Although oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, and ferroptosis have been identified as potential mechanisms underlying TIC, roles pyroptosis necroptosis under TIC never investigated. It has shown that inhibition acetylcholinesterase function by using donepezil exerts protective in various heart diseases. However, it remains unknown whether...