Effect of bushen tongluo decoction on the ERK/c-Fos signal transduction pathway in rats with bone cancer pain.

Bone cancer pain could lead to pain sensitization. Traditional Chinese Medicine could relieve bone cancer pain (BCP). This study aimed to investigate the analgesic effect of Bushen Tongluo decoction on rats with BCP and its impact on ERK/c-fos pathway in spinal dorsal horn. Cancer cells were injected to induce bone cancer pain rats. Inflammatory factors in serum were determined using enzyme-linked immunosorbent. ERK/c-Fos in the spinal dorsal horn were detected using western blotting and RT-qPCR. Thermal hyperalgesia and mechanical allodynia were observed in BCP rats. The ERK/c-Fos pathway activation was observed in the spinal dorsal horn and the expression of inflammatory cytokines increased in the serum. Bushen Tongluo decoction alleviated inflammatory cytokines and reduced the ERK/c-Fos pathway. We provided evidence that Bushen Tongluo decoction exhibits a potential and beneficial effect on inflammatory cytokines, effectively alleviating allodynia and hyperalgesia in rats with bone cancer. This effect may be attributed to down-regulation of the ERK/c-Fos pathway in spinal dorsal horn and serum inflammatory cytokines.

[Study on antagonistic effect of liangxue huayu recipe on endoplasmic reticulum stress-induced L02 hepatocyte apoptosis and its mechanism].

Endoplasmic reticulum stress (ERS) is a new pathway inducing cell apoptosis that has been discovered in recent years. This study focused on the protective effect of Liangxue Huayu recipe (LHR) on tumor necrosis factor-alpha (TNF-alpha) and D-GalN-induced hepatocyte apoptosis. It found that TNF-alpha and D-GalN could obviously inhibit hepatocyte proliferation, induce cell apoptosis, and significantly increase free calcium ions in cytoplasms, as well as protein expressions of ERS apoptosis-related signal molecules phosphorylated PERK, phosphorylated elF2alpha, cleaved Caspase-12, GRP78 and CHOP. After the administration of LHR of different concentrations, compared with the TNF-alpha/GalN injury group, LHR could significantly alleviated L02 hepatocyte proliferation, decreased cell apoptosis, inhibited growth of intracytoplasmic free calcium content, and gradually reduced the protein expressions of phosphorylated PERK, phosphorylated elF2alpha, cleaved Caspase-12, GRP78 and CHOP. These findings indicated that LHR has the inhibitory effect on TNF-alpha and D-GalN-induced hepatocyte apoptosis. Its mechanism may be related to down-regulation of ERS apoptosis-related signal molecules phosphorylated PERK, phosphorylated elF2alpha, cleaved Caspase-12, GRP78 and CHOP that maintain calcium homeostasis in endoplasmic reticulum.