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The heat exposure and white noise can induce damage on reproductive organs. The main objective of this study is to observe, if betanin administration could ameliorate oxidative stress, apoptosis and inflammation in testis of rodents following noise and scrotal hyperthermia exposure. Wistar rats were divided into 6 groups; control, betanin, noise, hyperthermia and two treatment groups. Scrotal hyperthermia model was performed by heat exposure of rat testicular (43 °C) for 15 min and 3 times per weeks for 14 days. Noise induction model was done following exposure of rats with 100-dB noise level for 14 days and 8 h daily similar to real exposure condition in human. Betanin was administrated at the sub-effective dose (15 mg/kg) by gavage route for 4 weeks (5 times a week) to male rats. The animals were euthanized and testis were dissected and stored at -80 °C. Then, the oxidative stress biomarkers (MDA and GSH), apoptosis (cytochrome & Annexin V), and inflammatory cytokines (TNF-α & IL-6) were measured by the real time polymerase chain reaction (RT-PCR) of testis collected samples. The data output demonstrates the impact of noise and hyperthermia in testicular toxicity induction by mitigating oxidative damage, apoptosis and inflammatory mediators. Following treatment with 15 mg/kg per day of betanin, lipid peroxidation and GSH content have been modulated, and TNF-α and IL-6 gene expression has been declined. Our results revealed that in Wistar rats, betanin displays protective effects against noise and scrotal hyperthermia-induced acute testicular toxicity through the inhibition of oxidative stress, apoptosis, and inflammation.
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http://dx.doi.org/10.1016/j.heliyon.2024.e38289 | DOI Listing |
Chem Biodivers
September 2025
Department of Pharmaceutical Analysis, School of Pharmacy, Hebei Medical University, Shijiazhuang, People's Republic of China.
Usnic acid, a compound from Usneae Filum, has shown notable antitumor effects. Nevertheless, the mechanism of its anti-NSCLC action remains incompletely elucidated. This study used metabolomics, network pharmacology, molecular docking, and dynamics simulation to investigate usnic acid's potential mechanism on NSCLC utilizing A549 cell samples.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Nephrology, Chungnam National University, Daejeon, Republic of Korea.
Diabetic kidney disease (DKD) involves oxidative stress-driven damage to glomeruli (Gloms) and proximal convoluted tubules (PCT). NAD(P)H: quinone oxidoreductase 1 (NQO1) regulates redox balance, but its compartment-specific role remains unclear. Streptozotocin (STZ)-induced hyperglycemia increased albuminuria and foot process effacement, with NQO1 KO (NKO) mice exhibiting greater podocyte injury than WT, indicating exacerbated glomerular damage.
View Article and Find Full Text PDFBackground: Anemia is common in hemodialysis patients, and iron supplementation is essential for its management. However, the impact of baseline inflammation on the efficacy of oral versus intravenous iron remains unclear.
Methods: This post hoc analysis of the IHOPE trial included 193 maintenance hemodialysis patients stratified by median baseline high-sensitivity C-reactive protein (hsCRP).
J Infect Dis
September 2025
Section of Infectious Diseases, Yale School of Medicine, New Haven, CT, USA.
Background: Women are disproportionately affected by neuropsychiatric symptoms following recovery from acute COVID-19. However, whether there are central nervous system-specific changes in gene expression in women with neuropsychiatric Long COVID (NP-Long COVID) remains unknown.
Methods: Twenty-two women with and ten women without NP-Long COVID were enrolled from New Haven, CT, and the surrounding region and consented to a blood draw and large volume lumbar puncture.
J Vis Exp
August 2025
Department of Cardiology, First Hospital of Nanping City affiliated to Fujian Medical University;
Myocardial ischemia-reperfusion injury (MIRI) endures as a substantial impediment to the management of cardiovascular disease. The pathophysiology of MIRI is complex, involving oxidative stress, calcium overload, inflammation, and apoptosis. The NRG1/ErbB4 signaling pathway has been implicated in modulating oxidative stress responses in the heart, potentially reducing cellular damage caused by free radicals.
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