CORM-2 prevents human gingival fibroblasts from lipoteichoic acid-induced VCAM-1 and ICAM-1 expression by inhibiting TLR2/MyD88/TRAF6/PI3K/Akt/ROS/NF-κB signaling pathway.

Periodontal diseases are prevalent worldwide. Lipoteichoic acid (LTA), a major component of gram-positive bacteria, may play a key role in periodontally inflammatory diseases. Carbon monoxide (CO) is a critical messenger in many biological processes. It can elicit various biological properties, especially anti-inflammatory effects. As the straight administration of CO remains difficult, CO-releasing molecules (CO-RMs) are emerging as promising alternatives. To explore the pharmacological actions and signaling pathways of CO battling LTA-induced periodontal inflammation, this study investigated the cytoprotective effects of CORM-2 against the adhesion of THP-1 monocytes to human gingival fibroblasts (HGFs) and the underlying molecular mechanism. After exposing HGFs to LTA with or without CORM-2 pretreatment, monocyte adhesion was determined. VCAM-1 and ICAM-1 expression in HGFs was measured by real-time PCR. To identify the signaling pathways of CO involved in the cytoprotective effects of CORM-2, HGFs underwent pharmacological or genetical interventions before LTA incubation. The expression and/or activity of possible regulatory molecules were determined. The release of pro-inflammatory cytokines, including IL-1ß, IL-6, and TNF-α, were measured using ELISA. The results showed that LTA increased cytokine production and upregulated VCAM-1 and ICAM-1 expression in HGFs, promoting monocyte adhesion. These events were dependent on TLR2/MyD88/TRAF6- and PI3K/Akt/NADPH oxidase/ROS-regulated NF-κB activation. CORM-2 inhibited LTA-induced inflammatory cascades in HGFs, in which CO seemed to be the hitman. To conclude, CO released from CORM-2 can prevent the LTA-stimulated HGFs from increasing VCAM-1 and ICAM-1 expression and promoting monocyte adhesion by inhibiting TLR2/MyD88/TRAF6 association and PI3K/Akt/NADPH oxidase/ROS signaling, both converge on the canonical NF-κB activation.

Early intervention combining Chinese and Western medicine in traumatic brain injury with diffuse axonal injury: A report of three cases.

BACKGROUND: Traumatic brain injury (TBI) is characterized by high prevalence, morbidity, and mortality. Diffuse axonal injury (DAI) is a specific type of TBI leading to prolonged consciousness impairment and disability. There is still no standard treatment for DAI, so we introduced traditional Chinese medicine into the treatment of these patients. CASE SUMMARIES: Three patients had TBI after traffic accidents. Their Glasgow Coma Scale (GCS) scores in the intensive care unit (ICU) were E1VEM2-3, E1VEM2-3, and E1VEM2 respectively. All of them were diagnosed with DAI based on magnetic resonance imaging (MRI). Because of continuing consciousness disturbances, their families agreed to combine traditional Chinese medicine and modern medicine treatments through inpatient consultation in Taoyuan General hospital. Two patients took Buyang Huanwu Decoction, and one Tianma Gouteng Decoction twice a day. All of them received 20 min of acupuncture treatments 5 times per week. Acupuncture points included Baihui (GV20), Sishencong (EX-HN1), Shuigou (GV26), Hegu (LI4), and Taichong (LR3). All of them started Traditional Chinese medicine treatment within 2 weeks after TBI. The GCS of all three patients recovered to E4M5V6. CONCLUSIONS: The early addition of traditional Chinese medicine treatments to Western medical care can improve the prognosis of patients with diffuse axonal injury.