METHODS: A comprehensive literature review was conducted, followed by in-depth interviews with key informants. Content analysis was performed to summarize the role of health equity in HTA in 13 health systems in Asia, including Brunei Darussalam, Cambodia, China, Indonesia, Japan, Malaysia, Myanmar, Philippines, Singapore, South Korea, Taiwan, Thailand, and Vietnam.
RESULTS: Health equity was reported to be considered in most health systems' HTA processes, except for Cambodia and Myanmar, which do not have an established HTA process. Interviews revealed that health equity has been more frequently considered to address the unmet medical needs of specific diseases (eg, high disease burden or severity, rare diseases, cancer, and diseases affecting children and the elderly) in Brunei Darussalam, China, Japan, Malaysia, Singapore, South Korea, Taiwan, Thailand, and Vietnam or inequities in socially disadvantaged groups (eg, socioeconomic status and geographical location) in Indonesia and the Philippines. Equity-informative economic evaluation was still in the early stages, with only 3 health systems reporting their use.
CONCLUSIONS: Health equity is considered in the HTA process in most Asian health systems. However, quantitative evaluation of health equity impact is still in its infancy because few health systems have just begun to perform equity-informative economic evaluations.
AIM OF THE STUDY: The molecular mechanisms of the anti-inflammatory properties of M. accedens are not yet understood. Therefore, we examined those mechanisms using a methanol extract of M. accedens (Ma-ME) and determined the target molecule in macrophages.
MATERIALS AND METHODS: We evaluated the anti-inflammatory effects of Ma-ME in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and in an HCl/EtOH-triggered gastritis model in mice. To investigate the anti-inflammatory activity, we performed a nitric oxide (NO) production assay and ELISA assay for prostaglandin E2 (PGE2). RT-PCR, luciferase gene reporter assays, western blotting analyses, and a cellular thermal shift assay (CETSA) were conducted to identify the mechanism and target molecule of Ma-ME. The phytochemical composition of Ma-ME was analyzed by HPLC and LC-MS/MS.
RESULTS: Ma-ME suppressed the production of NO and PGE2 and the mRNA expression of proinflammatory genes (iNOS, IL-1β, and COX-2) in LPS-stimulated RAW264.7 cells without cytotoxicity. Ma-ME inhibited NF-κB activation by suppressing signaling molecules such as IκBα, Akt, Src, and Syk. Moreover, the CETSA assay revealed that Ma-ME binds to Syk, the most upstream molecule in the NF-κB signal pathway. Oral administration of Ma-ME not only alleviated inflammatory lesions, but also reduced the gene expression of IL-1β and p-Syk in mice with HCl/EtOH-induced gastritis. HPLC and LC-MS/MS analyses confirmed that Ma-ME contains various anti-inflammatory flavonoids, including quercetin, daidzein, and nevadensin.
CONCLUSIONS: Ma-ME exhibited anti-inflammatory activities in vitro and in vivo by targeting Syk in the NF-κB signaling pathway. Therefore, we propose that Ma-ME could be used to treat inflammatory diseases such as gastritis.