sodium-aescinate and Disease-Models--Animal

Sodium aescinate (SA), a natural plant extract, has been proven to provide neuroprotection in neurological diseases. However, its role and the underlying pathophysiological mechanisms in traumatic brain injury (TBI) are still not well understood. The present study was aimed to investigate the protective effects of SA in both in vivo and in vitro TBI models. Mice or neurons were randomly divided into control, TBI, TBI + vehicle and TBI + SA groups. Neurologic severity score (NSS) was used to evaluate the neurological impairment. Brain water content and lesion volume were used to assess the brain injury degree. Malondialdehyde (MDA) and glutathione peroxidase (GPx) levels were used to estimate oxidative stress. Western blot was used to determine the protein levels. Nissl and terminal deoxynucleotidyl transferase-mediated dUTP nick 3'-end labeling (TUNEL) staining were used to measure cell death and apoptosis. Our results revealed that treatment of SA could improve neurological function, decrease cerebral edema and attenuate brain lesion after TBI. Furthermore, administration of SA suppressed TBI-induced oxidative stress, neuron cell death and apoptosis. In addition, SA activated the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway after TBI. However, SA failed to provide neuroprotection following TBI in Nrf2

Topics: Animals; Antioxidant Response Elements; Brain; Brain Injuries; Brain Injuries, Traumatic; Disease Models, Animal; Male; Mice, Inbred ICR; Neurons; Neuroprotection; Neuroprotective Agents; NF-E2-Related Factor 2; Oxidative Stress; Saponins; Triterpenes

Aescin has many physiological functions that are highly relevant to spinal cord injury (SCI), including anti-inflammation, anti-oxidation, anti-oedema, and enhancing vascular tone. The present study investigated the putative therapeutic value of aescin in SCI, with a focus on its neuroprotective, anti-inflammatory, and anti-oxidative properties. Sodium aescinate (1.0mg/kg body weight) or equivalent volume of saline was administered 30min after injury by intravenous injection, with an additional dose daily for seven consecutive days after moderate SCI in rats. After contusion injury of the 8th thoracic (T8) spinal cord, aescin-treated rats developed less severe hind limb weakness than saline controls, as assayed by the Basso-Beattie-Bresnahan scale, the beam walking test, and a footprint analysis. The improved locomotor outcomes in aescin-treated rats corresponded to markedly decreased immune response, oxidative stress, neuronal loss, axon demyelination, spinal cord swelling, and cell apoptosis, measured around T8 after impact. Our data suggest aescin treatment as a novel, early, neuroprotective approach in SCI. Given the known safety of aescin in clinical applications, the results of this study suggest that it is a good candidate for SCI treatment in humans.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cell Death; Disease Models, Animal; Drug Administration Schedule; Injections, Intravenous; Locomotion; Male; Neurons; Neuroprotective Agents; Oxidative Stress; Rats; Rats, Sprague-Dawley; Recovery of Function; Saponins; Spinal Cord; Spinal Cord Injuries; Treatment Outcome; Triterpenes

Toll like receptor 2 (TLR2) signaling can regulate the pathogenesis of otitis media (OM). However, the precise role of TLR2 signaling in OM has not been clarified due to the lack of an optimal animal model. Peptidoglycan-polysaccharide (PGPS) of the bacterial cell wall can induce inflammation by activating the TLR2 signaling. This study aimed at examining the pathogenic characteristics of OM induced by PGPS in Tlr2(-/-) mice, and the potential therapeutic effect of sodium aescinate (SA) in this model.. Wild-type (WT) and Tlr2(-/-) mice were inoculated with streptococcal PGPS into their middle ears (MEs) and treated intravenously with vehicle or SA daily beginning at 3days prior to PGPS for 6 consecutive days. The pathologic changes of individual mice were evaluated longitudinally.. In comparison with WT mice, Tlr2(-/-) mice were susceptible to PGPS-induced OM. Tlr2(-/-) mice displayed greater hearing loss, tympanic membrane damage, ME mucosal thickening, longer inflammation state, cilia and goblet cell loss. SA-treatment decreased neutrophil infiltration, modulated TLR2-related gene expression and improved ciliary organization.. PGPS induced a relatively stable OM in Tlr2(-/-) mice, providing a new model for OM research. Treatment with SA mitigated the pathogenic damage in the ME and may be valuable for intervention of OM.

Topics: Administration, Intravenous; Animals; Disease Models, Animal; Drug Administration Schedule; Female; Humans; Male; Mice; Mice, Inbred C57BL; Otitis Media; Peptidoglycan; Saponins; Signal Transduction; Toll-Like Receptor 2; Triterpenes