Anisomeles indica Extracts and Their Constituents Suppress the Protein Expression of ACE2 and TMPRSS2 In Vivo and In Vitro.

Coronavirus disease 2019 (COVID-19), stemming from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has had a profound global impact. This highly contagious pneumonia remains a significant ongoing threat. Uncertainties persist about the virus's effects on human health, underscoring the need for treatments and prevention. Current research highlights angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) as key targets against SARS-CoV-2. The virus relies on ACE2 to enter cells and TMPRSS2 to activate its spike protein. Inhibiting ACE2 and TMPRSS2 expression can help prevent and treat SARS-CoV-2 infections. Anisomeles indica (L.) Kuntze, a medicinal plant in traditional Chinese medicine, shows various promising pharmacological properties. In this study, ethanolic extracts of A. indica were examined both in vivo (250 and 500 µM) and in vitro (500 µM). Through Western blotting analysis, a significant reduction in the expression levels of ACE2 and TMPRSS2 proteins was observed in HepG2 (human hepatocellular carcinoma) cells and HEK 293T (human embryonic kidney) cell lines without inducing cellular damage. The principal constituents of A. indica, namely, ovatodiolide (5 and 10 µM), anisomlic acid (5 and 10 µM), and apigenin (12.5 and 25 µM), were also found to produce the same effect. Furthermore, immunohistochemical analysis of mouse liver, kidney, and lung tissues demonstrated a decrease in ACE2 and TMPRSS2 protein expression levels. Consequently, this article suggests that A. indica and its constituents have the potential to reduce ACE2 and TMPRSS2 protein expression levels, thus aiding in the prevention of SARS-CoV-2 infections.

Botanical Antcin K Alleviates High-Fat Damage in Palm Acid Oil-Treated Vascular Endothelial Cells and Macrophages.

Lipid metabolism disorder is the most critical risk factor for atherosclerosis, and the process involves lipid deposition in the arterial intima. In Taiwan, antcin K, an active triterpenoid from the fruiting bodies of Antrodia camphorata, has been considered a potential lipid-lowering agent. Despite this, the possible therapeutic mechanisms of antcin K remain unclear. To explore the crucial role of botanical antcin K in reducing atherosclerotic plaque, we used SVEC4-10 vascular endothelial cells and RAW264.7 macrophages with palm acid oil-induced high-fat damage as our cell models. Our results showed through using the DPPH assay that antcin K had excellent free radical scavenging ability. Antcin K treatment can significantly alleviate the high-fat damage and reduce the levels of inflammatory factors of TNF-α and IL-1ß in vascular endothelial cells and macrophages, as shown through MTT assay and ELISA. Furthermore, antcin K treatment can effectively enhance migration ability and clear lipid deposition in macrophages, as shown by using cell migration assay and oil red O staining. When stained with immunofluorescence, antcin K was shown to significantly decrease the expression of adhesion molecules of vascular cell adhesion molecule 1 (VCAM-1) in vascular endothelial cells involved in monocyte migration and inflammation. Antcin K not only reduced the expression of the CD36 scavenger receptor but also augmented the expression of Kruppel-like factor 4 (KLF4) transcription factor in macrophages, which inhibits the transformation of macrophages into foam cells underlying the pathological process of atherosclerosis. Taking our findings into account, we suggested that botanical antcin K could have therapeutic potential for the treatment of atherosclerosis.