Topic: HMGB1

Vincristine (VCR), an anticancer drug, frequently causes chemotherapy-induced peripheral neuropathy (CIPN). We have reported that macrophages (Mφ)-derived HMGB1 is involved in CIPN induced by paclitaxel in mice, whereas the mechanisms for VCR-induced CIPN (VIPN) remain unclear. We thus examined whether VIPN involves HMGB1 derived from Mφ or Schwann cells in mice. VCR at 0.2 mg/kg was administrated i.p. to mice daily for 10 days with a 2-day break, and nociceptive threshold at the hindpaw was evaluated by von Frey test. An anti-HMGB1-neutralizing antibody (HMGB1-Ab), soluble thrombomodulin (TMα

Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting adverse reactions in chemotherapy with cytotoxic anticancer agents. We have demonstrated that CIPN caused by paclitaxel involves high mobility group box 1 (HMGB1), a nuclear protein, derived from macrophages (Mφ) in laboratory animals (Neuropharmacology 141, 201, 2018), and that postmenopausal estrogen decline aggravates CIPN in patients undergoing paclitaxel-based chemotherapy (J Pharmacol Sci 146, 49, 2021). In this study, we analyzed estrogen modulation of upstream and downstream mechanisms of HMGB1. Female mice were subje

Background: Epilepsy and seizures occurrence are closely interwoven with brain inflammation. The inflammatory response is largely mediated by microglia, which are under strong circadian regulation. Circadian rhythms are 24-hour variations in physiological function orchestrated by a network of autoregulatory genes, including its key component, Bmal1. Here we explored the impact of Bmal1 knock down in microglial cells on seizure susceptibility and the CNS-immune profile.Methods: Forty young adult Bmal1-Cx3CR1Cre-ER mice were injected with either tamoxifen (40 mg/kg; IP; daily for 10 days) to ind