OBJECTIVE: To study changes in the nuclear factor-κB p65 (NF-κB p65)-inducible nitric oxide synthase (iNOS)-nitric oxide (NO) signaling pathway and the effects of Xinfeng capsules (XFC) in patients with ankylosing spondylitis (AS). METHODS:One hundred twenty patients with AS were randomly divided into an XFC group and a Salazopyrin group. Sixty health subjects were included as a normal control group. In the two treatment groups, pulmonary functional parameters, forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), maximal voluntary ventilation (MVV), peak expiratory flow (PEF), forced expiratory flow at 25% of forced vital capacity (FEF25), forced expiratory flow at 50% of forced vital capacity (FEF50), and forced expiratory flow at 75% of forced vital capacity (FEF75) were determined. Enzyme linked immunosorbent assays were used for detection of the serum oxidative stress indexes, NF-κB p65, iNOS, NO, reactive oxygen species (ROS), reactive nitrogen species (RNS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), total antioxidative capacity (TAOC) and interleukin-4 (IL-4), IL-10, IL-1β, and tumor necrosis factor-α (TNF-α) contents. Westergren's method was used for determination of erythrocyte sedimentation rate (ESR). High-sensitivity C-reactive protein (Hs-CRP) was detected with a 7060 full-automatic biochemical analyzer (Hitachi, Japan). RESULTS: The clinical therapeutic effect in the XFC group was significantly superior to that in the Salazopyrin group (P < 0.01). Compared with the normal control group, FEV1, MVV, PEF, FEF50, FEF75, SOD, CAT, TAOC, IL-4, IL-10 were significantly lower, and NF-κB p65, iNOS, NO, ROS, RNS, MDA, IL-1β, TNF-α, ESR, and Hs-CRP significantly higher in patients with AS (P < 0.01 or P < 0.05). Compared with before treatment, FEV1, MVV, PEF, FEF50, FEF75, SOD, CAT, TAOC, IL-4, and IL-10 were significantly increased, and NF-κB p65, iNOS, NO, ROS, RNS, MDA, IL-1β, TNF-α, ESR, CRP, visual analog scales (VAS), Bath ankylosing spondylitis disease active index, Bath ankylosing spondylitis functional index, and Bath ankylosing spondylitis global index significantly decreased in the two treatment groups after treatment (P <. 0.01 or P < 0.05), with significant differences between the XFC and Salazopyrin groups (P < 0.01 or P < 0.05). Spearman correlation analysis indicated that FEV1, MWVV, PEF, FEF50, and FEF75 were positively correlated with SOD, CAT, TAOC, IL-4, and IL-10, and were negatively correlated with NF-κB p65, iNOS, NO, ROS, RNS, MDA, IL-13, TNF-α, ESR, and CRP. CONCLUSION: Patients with AS have local pathologic changes in the spinal cord and other joints. They also have decreased pulmonary function, which is negatively correlated with the NF-κB-iNOS-NO signaling pathway, oxidative indexes, and inflammatory factors. XFC improves rigidity and pain in spinal joints and other symptoms, laboratory indexes, and pulmonary function. The mechanism is possibly related to inhibition of the NF-KB-iNOS-NO signaling pathway.
RCT Entities:
OBJECTIVE: To study changes in the nuclear factor-κB p65 (NF-κB p65)-inducible nitric oxide synthase (iNOS)-nitric oxide (NO) signaling pathway and the effects of Xinfeng capsules (XFC) in patients with ankylosing spondylitis (AS). METHODS: One hundred twenty patients with AS were randomly divided into an XFC group and a Salazopyrin group. Sixty health subjects were included as a normal control group. In the two treatment groups, pulmonary functional parameters, forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), maximal voluntary ventilation (MVV), peak expiratory flow (PEF), forced expiratory flow at 25% of forced vital capacity (FEF25), forced expiratory flow at 50% of forced vital capacity (FEF50), and forced expiratory flow at 75% of forced vital capacity (FEF75) were determined. Enzyme linked immunosorbent assays were used for detection of the serum oxidative stress indexes, NF-κB p65, iNOS, NO, reactive oxygen species (ROS), reactive nitrogen species (RNS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), total antioxidative capacity (TAOC) and interleukin-4 (IL-4), IL-10, IL-1β, and tumor necrosis factor-α (TNF-α) contents. Westergren's method was used for determination of erythrocyte sedimentation rate (ESR). High-sensitivity C-reactive protein (Hs-CRP) was detected with a 7060 full-automatic biochemical analyzer (Hitachi, Japan). RESULTS: The clinical therapeutic effect in the XFC group was significantly superior to that in the Salazopyrin group (P < 0.01). Compared with the normal control group, FEV1, MVV, PEF, FEF50, FEF75, SOD, CAT, TAOC, IL-4, IL-10 were significantly lower, and NF-κB p65, iNOS, NO, ROS, RNS, MDA, IL-1β, TNF-α, ESR, and Hs-CRP significantly higher in patients with AS (P < 0.01 or P < 0.05). Compared with before treatment, FEV1, MVV, PEF, FEF50, FEF75, SOD, CAT, TAOC, IL-4, and IL-10 were significantly increased, and NF-κB p65, iNOS, NO, ROS, RNS, MDA, IL-1β, TNF-α, ESR, CRP, visual analog scales (VAS), Bath ankylosing spondylitis disease active index, Bath ankylosing spondylitis functional index, and Bath ankylosing spondylitis global index significantly decreased in the two treatment groups after treatment (P <. 0.01 or P < 0.05), with significant differences between the XFC and Salazopyrin groups (P < 0.01 or P < 0.05). Spearman correlation analysis indicated that FEV1, MWVV, PEF, FEF50, and FEF75 were positively correlated with SOD, CAT, TAOC, IL-4, and IL-10, and were negatively correlated with NF-κB p65, iNOS, NO, ROS, RNS, MDA, IL-13, TNF-α, ESR, and CRP. CONCLUSION:Patients with AS have local pathologic changes in the spinal cord and other joints. They also have decreased pulmonary function, which is negatively correlated with the NF-κB-iNOS-NO signaling pathway, oxidative indexes, and inflammatory factors. XFC improves rigidity and pain in spinal joints and other symptoms, laboratory indexes, and pulmonary function. The mechanism is possibly related to inhibition of the NF-KB-iNOS-NO signaling pathway.
Authors: Andrea Regel; Alexandre Sepriano; Xenofon Baraliakos; Désirée van der Heijde; Jürgen Braun; Robert Landewé; Filip Van den Bosch; Louise Falzon; Sofia Ramiro Journal: RMD Open Date: 2017-01-27