Corrigendum: Inhibitory effects of Rhaponticin on osteoclast formation and resorption by targeting RANKL-induced NFATc1 and ROS activity.

[This corrects the article DOI: 10.3389/fphar.2021.645140.].

Inhibitory Effects of Rhaponticin on Osteoclast Formation and Resorption by Targeting RANKL-Induced NFATc1 and ROS Activity.

The extravagant osteoclast formation and resorption is the main cause of osteoporosis. Inhibiting the hyperactive osteoclastic resorption is considered as an efficient treatment for osteoporosis. Rhaponticin (RH) is a small molecule that has been reported to possess anti-inflammatory, anti-allergic, anti-fibrotic, and anti-diabetic activities. However, the influence of RH on osteoclasts differentiation and function is still unclear. To this end, an array of assays including receptor activator of nuclear factor kappa-Β (NF-κB) ligand (RANKL) induced osteoclastogenesis, tartrate-resistant acidic phosphatase (TRAcP) staining, immunofluorescence, and hydroxyapatite resorption were performed in this study. It was found that RH had significant anti-catabolic effects by inhibiting osteoclastogenesis and bone resorption without cytotoxicity. Mechanistically, the expression of NADPH oxidase 1 (Nox1) was found to be suppressed and antioxidant enzymes including catalase, superoxide dismutase 2 (SOD-2), and heme oxygenase-1(HO-1) were enhanced following RH treatment, suggesting RH exhibited antioxidant activity by reducing the generation of reactive oxygen species (ROS) as well as enhancing the depletion of ROS. In addition, MAPKs, NF-κB, and intracellular Ca2+ oscillation pathways were significantly inhibited by RH. These changes led to the deactivation of osteoclast master transcriptional factor-nuclear factor of activated T cells 1 (NFATc1), as examined by qPCR and Western blot assay, which led to the decreased expression of downstream integrin ß3, c-Fos, cathepsin K, and Atp6v0d2. These results suggested that RH could effectively suppress RANKL-regulated osteoclast formation and bone resorption. Therefore, we propose that RH can represent a novel natural small molecule for the treatment of osteoporosis by inhibiting excessive osteoclast activity.

Median nerve compression caused by superficial brachial artery: an unusual clinical case.

An iatrogenic pseudoaneurysm of the radial artery and spontaneous venous malformation are associated with median nerve compression. However, the superficial brachial artery (SBA) has rarely been described as the cause of neurological deficits due to median nerve compression. A 61-year-old man was admitted to our clinic with a 1-year history of intermittent aching palsy in the left thumb that had progressed to the first three fingers. Clinical examination revealed mild sensory disturbance and hyperpathia in the first three fingers and weakness of the opponens pollicis. Ultrasound and magnetic resonance imaging confirmed that the SBA was compressing the median nerve by almost one-third. When anomalies of the SBA impinge on the median nerve, pulsatile pressure is applied to the nerve trunk. This may trigger ectopic stimulation of sensory fibers, leading to severe pain, sensory neuropathy, and motor disturbance. Considering the substantial difficulties and risks of a surgical operation as well as the patient's wish to undergo conservative treatment, we performed muscle relaxation and acupuncture to relieve the pressure of the surrounding soft tissue and in turn decrease the impingement of the SBA on the median nerve. A satisfactory treatment effect was reached in this case.