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Heat stress stimulates the production of reactive oxygen species (ROS), which cause oxidative damage in the kidney. This study clarifies the mechanism by which saikosaponin-d (SSd), which is extracted from the roots of Bupleurum falcatum L, protects heat-stressed pig kidney proximal tubular (LLC-PK₁) cells against oxidative damage. SSd alone is not cytotoxic at concentrations of 1 or 3 μg/mL as demonstrated by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To assess the effects of SSd on heat stress-induced cellular damage, LLC-PK₁ cells were pretreated with various concentrations of SSd, heat stressed at 42°C for 1 h, and then returned to 37°C for 9 h. DNA ladder and MTT assays demonstrated that SSd helped to prevent heat stress-induced cellular damage when compared to untreated cells. Additionally, pretreatment with SSd increased the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) but decreased the concentration of malondialdehyde (MDA) in a dose-dependent manner when compared to controls. Furthermore, real-time PCR and Western blot analysis demonstrated that SSd significantly increased the expression of copper and zinc superoxide dismutase (SOD-1), CAT, GPx-1 and heat shock protein 72 (HSP72) at both the mRNA and protein levels. In conclusion, these results are the first to demonstrate that SSd ameliorates heat stress-induced oxidative damage by modulating the activity of anti-oxidant enzymes and HSP72 in LLC-PK₁ cells.

Intense sound exposure causes permanent hearing loss due to hair cell and cochlear damage. Prior conditioning with sublethal stressors, such as non-traumatic sound, heat stress and restraint protects ear from acoustic injury. To explore the mechanisms of conditioning-induced cochlear protection, Young's modulus and the amount of filamentous actin (F-actin) of mouse outer hair cells (OHCs) with heat stress and those without such stress were investigated by atomic force microscopy (AFM) and confocal laser scanning microscopy (CLSM), respectively. Heat stress caused an increase in Young's modulus of OHCs at 3–6 h after its application along with an increase in their amount of F-actin. These time courses are similar to the previous report in which heat stress was shown to suppress permanent threshold shift. These results indicate that heat stress structurally modifies OHCs to increase their F-actin and thereby renders them stiffer, resulting in protection of ear from acoustic injury.