Introduction Numerous efforts in natural product drug development are reported for the treatment of Coronavirus. Based on the literature, among these natural plants Artemisia annua L. shows some promise for the treatment of SARS‐CoV‐2. Objective The main objective of our study was to determine artemisinin content by liquid chromatography electrospray ionisation tandem mass spectrometry (LC‐ESI‐MS/MS), to investigate the in vitro biological activity of artemisinin from the A. annua plants grown in Turkey with various extracted methods, to elaborate in silico activity against SARS‐CoV‐2 using molecular modelling. Methodology Twenty‐one different extractions were applied. Direct and sequential extractions studies were compared with ultrasonic assisted maceration, Soxhlet, and ultra‐rapid determined artemisinin active molecules by LC‐ESI‐MS/MS methods. The inhibition of spike protein and main protease (3CL) enzyme activity of SARS‐CoV‐2 virus was assessed by time resolved fluorescence energy transfer (TR‐FRET) assay. Results Artemisinin content in the range 0.062–0.066%. Artemisinin showed significant inhibition of 3CL protease activity but not Spike/ACE‐2 binding. The 50% effective concentration (EC50) of artemisinin against SARS‐CoV‐2 Spike pseudovirus was found greater than 50 μM (EC45) in HEK293T cell line whereas the cell viability was 94% of the control (P < 0.01). The immunosuppressive effects of artemisinin on TNF‐α production on both pseudovirus and lipopolysaccharide (LPS)‐induced THP‐1 cells were found significant in a dose dependent manner. Conclusion Further studies of these extracts for COVID‐19 treatment will shed light to seek alternative treatment options. Moreover, these natural extracts can be used as an additional treatment option with medicines, as well as prophylactic use can be very beneficial for patients.

Aberrant expression of MEG3 has been shown in various cancers. The purpose of this study is to evaluate the effect of MEG3 on glioma cells including U87MG and patient-derived primary tumors cells and compare with nonglial HUVEC cells. Cell viability, migration and chemo sensitivity was assayed. Apoptosis was evaluated in MEG3 overexpressing and MEG3 suppressed cells. MEG3 expression was compared in patient-derived tumor cells with respect to IDH1 mutation status and WHO-grades. Silencing of MEG3 inhibited cell proliferation and reduced cell migration while overexpression of MEG3 promoted cell proliferation in glioma cells. MEG3 inhibition improved chemo sensitivity of glioma cells to 5-fluorouracil(5FU) but not to navitoclax. Suppression of MEG3 gene in patient-derived oligodendroglioma cells also showed the same effect whereas glioblastoma cell proliferation and chemo sensitivity were not affected by MEG3 inhibition. Further, cell death mechanism of action was found as apoptosis. Although MEG3 is a widely known tumor suppressor gene and its loss is associated with several cancer types, here we reported that MEG3 inhibition can be used in drug sensitivity for improving efficiency of known chemotherapeutics. We propose that the level of MEG3 should be evaluated in treatment of different glioma subtypes that are resistant to effective drugs.

Aberrant expression of MEG3 has been shown in various cancers. The purpose of this study is to evaluate the effect of MEG3 on glioma cells including U87MG and patient-derived primary tumors cells and compare with nonglial HUVEC cells. Cell viability, migration and chemo sensitivity was assayed. Apoptosis was evaluated in MEG3 overexpressing and MEG3 suppressed cells. MEG3 expression was compared in patient-derived tumor cells with respect to IDH1 mutation status and WHO-grades. Silencing of MEG3 inhibited cell proliferation and reduced cell migration while overexpression of MEG3 promoted cell proliferation in glioma cells. MEG3 inhibition improved chemo sensitivity of glioma cells to 5-fluorouracil(5FU) but not to navitoclax. Suppression of MEG3 gene in patient-derived oligodendroglioma cells also showed the same effect whereas glioblastoma cell proliferation and chemo sensitivity were not affected by MEG3 inhibition. Further, cell death mechanism of action was found as apoptosis. Although MEG3 is a widely known tumor suppressor gene and its loss is associated with several cancer types, here we reported that MEG3 inhibition can be used in drug sensitivity for improving efficiency of known chemotherapeutics. We propose that the level of MEG3 should be evaluated in treatment of different glioma subtypes that are resistant to effective drugs.