Publications by authors named "T Chunchai"
Article Synopsis
- The study investigates the role of the MD-2-TLR4 signaling pathway in cognitive decline related to obesity in male Wistar rats.
- Researchers used two MD-2 inhibitors, MAC28 and 2i-10, to explore their effects on cognitive impairment associated with a high-fat diet over 16 weeks.
- Blocking the MD-2-TLR4 pathway in obese rats improved cognitive function by reducing brain inflammation and damage, suggesting that targeting MD-2 could be a promising strategy for treating obesity-related cognitive decline.
This study aims to compare the efficacy of 5-alpha-reductase inhibitors (5ARIs) on anxiety and depression between long-term and short-term treatment followed by withdrawal in d-galactose (Dgal)-induced senescent male rats. Thirty-two, 8-week-old, male Wistar rats were divided into two groups: control rats and Dgal-treated rats (150 mg/kg/day; subcutaneously) for 18 weeks. At week 13, Dgal-treated rats were subdivided into three subgroups: (1) vehicle (DgV), (2) long-term treatment with 5ARIs, Finasteride 5 mg/kg/day, per oral for 6 weeks (DgF), (3) short-term treatment with 5ARIs, Finasteride 5 mg/kg/day, per oral for 2 weeks followed by a 4-week withdrawal period (DgW).
View Article and Find Full Text PDFInhibition of 5-alpha reductase attenuates cardiac oxidative damage in obese and aging male rats via the enhancement of antioxidants and the p53 protein suppression.
Chem Biol Interact
November 2024
In aging and metabolic syndrome oxidative stress is a causative factor in the cardiovascular pathology. Upregulation of 5-⍺ reductase is associated with cardiac hypertrophy but how inhibition of 5-⍺ reductase affects cardiometabolic function during oxidative damage under those conditions is unclear. Our hypothesis was that Finasteride (Fin), a 5-⍺ reductase inhibitor, promotes an antioxidant response, leading to an improvement in cardiac function in obese and aging rats.
View Article and Find Full Text PDFMuscarinic and nicotinic receptors stimulation by vagus nerve stimulation ameliorates trastuzumab-induced cardiotoxicity via reducing programmed cell death in rats.
Toxicol Appl Pharmacol
October 2024
Article Synopsis
- Trastuzumab, a treatment for certain cancers, can cause heart damage (cardiotoxicity), prompting concerns about its use due to limited heart cell regeneration.
- A study on male Wistar rats tested the effects of vagus nerve stimulation (VNS) on reducing this cardiotoxicity, discovering that VNS alleviated cardiac dysfunction and cell death caused by trastuzumab.
- The protective benefits of VNS were hindered by blocking specific acetylcholine receptors, indicating that VNS works by balancing autonomic activity and improving mitochondrial function in the heart.
Evidence concerning the osteotoxic effects of chemotherapy (doxorubicin) has been previously described. Periodontitis also progressively increases in patients receiving chemotherapy; however, the beneficial effects of melatonin and metformin on the alleviation of doxorubicin-induced osteotoxicity have never been investigated. Therefore, we investigated the negative impact of doxorubicin on alveolar bone homeostasis and the benefits of melatonin and metformin on the attenuation of doxorubicin-induced alveolar bone toxicity.
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