Department of Neurological Sciences, Rush University Medical Center, IL, Chicago, USA.
Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, Chicago, USA.
J Neuroimmune Pharmacol. 2021 Dec;16(4):743-755. doi: 10.1007/s11481-021-10028-1. Epub 2021 Oct 22.
Spike S1 of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) binds to angiotensin-converting enzyme 2 (ACE2) on host cells to enter the cell and initiate COVID-19. Since ACE2 is a favorable enzyme, we were interested in finding a molecule capable of binding spike S1, but not ACE2, and inhibiting the interaction between spike S1 and ACE2. Holy basil (Tulsi) has a long history as a medicine for different human disorders. Therefore, we screened different components of Tulsi leaf and found that eugenol, but not other major components (e.g. ursolic acid, oleanolic acid and β-caryophylline), inhibited the interaction between spike S1 and ACE2 in an AlphaScreen-based assay. By in silico analysis and thermal shift assay, we also observed that eugenol associated with spike S1, but not ACE2. Accordingly, eugenol strongly suppressed the entry of pseudotyped SARS-CoV-2, but not vesicular stomatitis virus (VSV), into human ACE2-expressing HEK293 cells. Eugenol also reduced SARS-CoV-2 spike S1-induced activation of NF-κB and the expression of IL-6, IL-1β and TNFα in human A549 lung cells. Moreover, oral treatment with eugenol reduced lung inflammation, decreased fever, improved heart function, and enhanced locomotor activities in SARS-CoV-2 spike S1-intoxicated mice. Therefore, selective targeting of SARS-CoV-2 spike S1, but not ACE2, by eugenol may be beneficial for COVID-19 treatment.
严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2)的刺突 S1 与宿主细胞上的血管紧张素转换酶 2 (ACE2)结合,进入细胞并引发 COVID-19。由于 ACE2 是一种有利的酶,我们有兴趣寻找一种能够结合刺突 S1 但不结合 ACE2 的分子,并抑制刺突 S1 与 ACE2 之间的相互作用。圣罗勒(Tulsi)作为治疗人类不同疾病的药物已有很长的历史。因此,我们筛选了圣罗勒叶的不同成分,发现丁香酚,但不是其他主要成分(如熊果酸、齐墩果酸和β-石竹烯),在基于 AlphaScreen 的测定中抑制了刺突 S1 与 ACE2 的相互作用。通过计算机分析和热移位测定,我们还观察到丁香酚与刺突 S1 结合,但不与 ACE2 结合。因此,丁香酚强烈抑制假型 SARS-CoV-2 进入人 ACE2 表达的 HEK293 细胞,但不抑制水疱性口炎病毒(VSV)。丁香酚还降低了 SARS-CoV-2 刺突 S1 诱导的人 A549 肺细胞中 NF-κB 的激活和 IL-6、IL-1β 和 TNFα 的表达。此外,口服丁香酚可减轻 SARS-CoV-2 刺突 S1 中毒小鼠的肺部炎症,降低发热,改善心脏功能,并增强运动活动。因此,丁香酚选择性靶向 SARS-CoV-2 刺突 S1,而不是 ACE2,可能有益于 COVID-19 的治疗。