Notoginsenoside R1 improves monocrotaline-induced pulmonary arterial hypertension via modulation NF-κB signaling in rats
Purpose: To investigate the potentials of notoginsenoside R1 (NGR1) in ameliorating inflammation and pulmonary vascular remodeling in rats with pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT), and to examine the mechanisms underlying such effects.
Methods: Eight-week-old male Sprague Dawley rats were randomly divided into groups: control, MCT, MCT+5mg/kg NGR1, MCT+12.5mg/kg NGR1, and MCT + 25 mg/kg NGR1. Right cardiac catheterization was used to measure pulmonary hemodynamics. Pulmonary morphology was evaluated with the aid of H & E staining. Serum levels of inflammatory cytokines were measured using ELISA, while levels of inflammation-associated factors in the lung were measured using RT-PCR. NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) and IκBα (nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha) protein levels were determined by western blot.
Results: Pulmonary hemodynamics and pulmonary morphology worsened following MCT injection and were accompanied by NF-κB pathway activation and elevated levels of inflammation-associated factors. In contrast, MCT treatment followed by NGR1 treatment ameliorated MCT-induced PAH by improving pulmonary hemodynamics and pulmonary vascular remodeling while reducing NF-κB activation and levels of inflammation-associated factors.
Conclusion: NGR1 exerts ameliorative effects on MCT-induced PAH by inhibiting NF-κB pathway. Therefore, NGR1 may be a new potential therapy for PAH.
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