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SARS-CoV-2 Omicron led to the most serious outbreak of COVID-19 in Hong Kong in 2022. Under the pressure of a high volume of patients and limited medical resources, Chinese herbal medicine (CHM) has been extensively used. This is a case-control study of the infected patients that aims to evaluate the effectiveness of CHM using data extracted from the Hong Kong Baptist University Telemedicine Chinese Medicine Centre database. Patients with COVID-19 confirmed by either a rapid antigen test or a polymerase chain reaction who had completed two consultations and taken CHM within 10 days of the first positive test were included in the study (CHM group, n = 3 1 1). The matched control cases were those who did not take CHM within 10 days of the first positive test and were based on age (± 3 years), vaccine doses (< 3 doses, or 3 doses), and gender (no-CHM group, n = 3 1 1). The outcomes included the negative conversion time (NCT, primary outcome), total score of individual symptoms, number of the reported symptoms, and individual symptom disappearance rates. The NCT of the CHM group (median days: 7.0, interquartile range: 6.0–8.0) was significantly shorter than that of the no-CHM group (8.0, 7.0–10.5; P = 0. 0 1 6). CHM treatment significantly reduced the total score of individual symptoms (P < 0. 0 0 1) and the number of the reported symptoms (P < 0. 0 0 1) as compared with that of the no-CHM group. Additionally, the symptom disappearance rates of symptoms such as chills, cough, sputum, dry throat, itching throat, headache, chest tightness, abdominal pain, diarrhea, and fatigue were significantly higher in the CHM group than in the no-CHM group. In conclusion, CHM intervention can significantly reduce NCT and COVID-19 symptoms. Chinese medicine can be accurately prescribed based on a telemedical consultation. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Ginseng (Panax ginseng C.A. Meyer) is widely used in Asian communities for treating cardiovascular diseases. However, the mechanism by which it protects the myocardium in ischemia–reperfusion (I/R) injury remains unclear. In this study, we aim to investigate whether a standardized ginseng extract (RSE) protects rodent hearts against I/R injury and if glucocorticoid and/or estrogen receptor-mediated activation of Akt and Erk1/2 (the reperfusion injury salvage kinase pathway, RISK) and subsequent nitric oxide (NO) synthesis signaling are involved in this effect. Materials and methods: Rats or gene-deleted mice were subjected to 30min ischemia by occluding the left anterior descending coronary artery and 90min reperfusion. Infarct size, serum level of creatine kinase (CK), lactate dehydrogenase (LDH), and NO, expression and phosphorylation of glucocorticoid receptor (GR), estrogen receptor (ER), phosphatidylinositol-3 kinase (PI3K), Akt, NO synthase (NOS), extracellular signal-regulated kinase (Erk) 1/2, p38, and c-Jun NH2 terminal kinases (JNK) were examined in rat or mice treated with or without RSE in the absence or presence of pharmacological inhibitors. Results: RSE significantly reduced infarct size in a dose-dependent manner and reduced the incidence of arrhythmia, increased serum NO production, reduced serum activities of creatine kinase and lactate dehydrogenase. The infarct size reduction effect of RSE was abolished by RU468 (an inhibitor of GR), tamoxifen (an inhibitor of ER), LY294002 (an inhibitor of PI3K), Akt inhibitor IV (an inhibitor of Akt protein kinase), U0126 (an inhibitor of Erk1/2) and NG-nitro-l-arginine methyl ester hydrochloride (an inhibitor of NOS), but not actinomycin D (an inhibitor of transcription process). RSE also significantly increased the activation of GR/ER, PI3K–Akt–eNOS cascades and Erk1/2 signaling in rat heart. However, RSE did not markedly reduce infarct size in endothelium NOS−/− mice. This differs from its effect in inducible NOS−/− and wild type mice, suggesting that endothelium NOS is required for the beneficial effect of RSE on the heart. Conclusion: Our findings showed for the first time that RSE protects hearts subjected to acute I/R injury and the infarct size reduction effect of RSE is associated with GR and/or ER-mediated Akt and Erk1/2 activation in an endothelium NOS-dependent manner. [Copyright &y& Elsevier]