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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Role of non-macrophage cell-derived HMGB1 in oxaliplatin-induced peripheral neuropathy and its prevention by the thrombin/thrombomodulin system in rodents: negative impact of anticoagulants

Fig. 1

Involvement of endogenous HMGB1 in the oxaliplatin (OHP)-induced neuropathic allodynia in rodents. a, b Preventive (a) and therapeutic (b) effects of an anti-HMGB1-neutralizing antibody (HMGB1-Ab) on the OHP-induced mechanical allodynia in mice. HMGB1-Ab or IgG at 1 mg/kg was administered i.p. 1 h before (a) or 8 days after i.p. administration of OHP at 5 mg/kg in mice. c, d The protein levels of HMGB1 in the plasma (c), dorsal root ganglion (d, left), sciatic nerve (d, middle), and hind paw (d, right) 5 h and day 3 and/or 8 after OHP treatment in mice. e Preventive effect of HMGB1-Ab on the OHP-induced mechanical hyperalgesia and allodynia in rats, as assessed by the paw pressure and von Frey tests, respectively. OHP at 5 mg/kg was administered i.p. every third day, four times in total, and HMGB1-Ab or non-immune IgG at 1 mg/kg was repeatedly administered i.p. 1 h before and 24 h after each dose of OHP, eight times in total, i.e., on days 0, 1, 3, 4, 6, 7, 9, and 10 of OHP treatment. f Plasma HMGB1 levels 5 h and day 3 or 12 after the onset of OHP treatment in rats. V, vehicle. Data show the mean with SEM for four (a), four to eight (b), five (c, left), eight to nine (c, right), and four to five (d) mice and for four to five (e), and five to six (f) rats. *P < 0.05, **P < 0.01 vs. vehicle in the vehicle-treated mice (a, b) or rats (e); †P < 0.05, ††P < 0.01 vs. IgG in the OHP-treated mice (a, b) or rats (e)

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