Protective effect of higenamine ameliorates collagen-induced arthritis through heme oxygenase-1 and PI3K/Akt/Nrf-2 signaling pathways

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Abstract
Existing in Ranunculaceae Aconitum and tomato, with the chemical name 1‑phydroxybenzyl‑1,2,3,4‑tetrahy‑droisoquinoline, higenamine is widely distributed in China. Higenamine's anti‑inflammatory, antioxidant and anti‑apoptotic effects have been identified in previous studies. The present study attempted to determine the protective effect of higenamine against collagen‑induced arthritis through heme oxygenase‑1 (HO‑1) and PI3K/Akt/Nrf‑2 signaling pathways. A type II collagen (CII)‑induced arthritis (CIA) model was established and clinical arthritis scores were used to appraise the curative effect of higenamine. Inflammatory reactions, oxidative damage and caspase‑3/9 activation were detected using specific ELISA kits. In addition, western blotting was used to evaluate the expression of HO‑1, Akt and Nrf‑2 protein in CII‑induced CIA mice. In CII‑induced CIA mice, the clinical arthritis scores, inflammatory reactions, oxidation damage and caspase‑3/9 activation were increased and activated. The results demonstrated that treatment with higenamine significantly reduced the elevation of clinical arthritis scores (P<0.01), and suppressed the promotion of inflammatory reactions, oxidation damage and caspase‑3/9 activation. Furthermore, higenamine significantly increased HO‑1 protein expression (P<0.01) and upregulated the PI3K/Akt/Nrf‑2 signal pathway in CII‑induced CIA mice. Collectively, it is concluded that higenamine protects against CII‑induced CIA through the induction of HO‑1 and the upregulation of the PI3K/Akt/Nrf‑2 signaling pathway. In conclusion, higenamine may be a beneficial drug for protecting against CIA.

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