beta lapachone/atrophy

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Beta-lapachone attenuates immobilization-induced skeletal muscle atrophy in mice.

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Skeletal muscle atrophy reduces quality of life and increases morbidity and mortality in patients with chronic conditions. Oxidative stress is a key factor contributing to skeletal muscle atrophy by altering both protein synthesis and protein degradation pathways. Beta-lapachone (Beta-L) is known to

Increased susceptibility of spinal muscular atrophy fibroblasts to camptothecin is p53-independent.

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BACKGROUND Deletion or mutation(s) of the survival motor neuron 1 (SMN1) gene causes spinal muscular atrophy (SMA). The SMN protein is known to play a role in RNA metabolism, neurite outgrowth, and cell survival. Yet, it remains unclear how SMN deficiency causes selective motor neuron death and

Fast dissolving β-lapachone particles and tablets: an approach using surface adsorption technique.

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BACKGROUND β-lapachone (βLAP) is obtained from natural resources with promising preliminary results against the etiologic agent of Chagas disease. βLAP activity is associated with generation of free radical and inhibition of nucleic acids and protein synthesis leading an outstanding antichagasic

β-Lapachone attenuates cognitive impairment and neuroinflammation in beta-amyloid induced mouse model of Alzheimer's disease.

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Oxidative stress and neuroinflammation are critically involved in amyloid beta (Aβ) induced cognitive impairments. β-Lapachone (β-LAP) is a natural activator of NAD(P)H quinone oxidoreductase 1 (NQO1) which has antioxidant and anti-inflammatory properties.This study investigated the effect of β-LAP

KL1333, a derivative of β-lapachone, protects against cisplatin-induced ototoxicity in mouse cochlear cultures.

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Cisplatin (CP) is a chemotherapeutic drug used to treat cancerous solid tumors, but it causes serious side effects, including ototoxicity. The major cause of CP-induced ototoxicity is increased levels of mitochondrial reactive oxygen species (ROS). In this study, we examined the effect of

Prevention of 1,2-dibromo-3-chloropropane (DBCP)-induced kidney necrosis and testicular atrophy by 3-aminobenzamide.

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The poly(ADP-ribosyl)transferase inhibitor, 3-aminobenzamide (3-ABA), reduced morphological evidence of 1,2-dibromo-3-chloropropane (DBCP)-induced DNA damage determined by alkaline elution. The DBCP plasma, kidney, and testis tissue doses determined between 1 and 8 hr after a single intraperitoneal

Inactivation of the SMN complex by oxidative stress.

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The SMN complex is essential for the biogenesis of small nuclear ribonucleoproteins (snRNPs), the major constituents of the spliceosome. Deficiency in functional SMN protein causes spinal muscular atrophy, a common motor neuron degenerative disease of severity commensurate with SMN levels and,

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