Traditional Chinese herb, Astragalus: possible for treatment and prevention of COVID-19?

Summary Astragalus is a traditional herb which has been used in China for a long time. It regulates blood circulation (vital energy), invigorates body fluid circulation, protects the flow of blood to fight against the attack of pathogens, and strengthens “blood deficiencies” according to Bencao Congxin. Astragalus was approved by the Food and Drug Administration in 2009 as a dietary supplement for upper respiratory infections, allergic rhinitis (hay fever), asthma, chronic fatigue syndrome, and chronic kidney disease. Thirty journals published in the past ten years were reviewed by using library search engines such as SCI/SCIE, PubMed, and Scopus. In this mini-review, we focus on the anti-inflammatory of Astragalus features, discuss the background of Astragalus and its function in various diseases from water-extracted Astragalus membranaceus, Astragalus saponins, and Astragalus polysaccharides. Based on the traditional Chinese medicine theory, Astragalus is a potential candidate to treat and prevent COVID-19.

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Anti-Inflammatory Function of Nodosin via Inhibition of IL-2

The American Journal of Chinese Medicine ◽

10.1142/s0192415x10007713 ◽

2010 ◽

Vol 38 (01) ◽

pp. 127-142 ◽

Cited By ~ 9

Author(s):

Jiyu Li ◽

Junming Du ◽

Lijuan Sun ◽

Jianwen Liu ◽

Zhiwei Quan

Keyword(s):

Clinical Trial ◽

T Lymphocytes ◽

Mrna Level ◽

Chinese Herb ◽

Potential Candidate ◽

Traditional Chinese Herb ◽

Anti Inflammatory ◽

Cell Mitosis ◽

Herb Medicine ◽

Chinese Herb Medicine

In order to explore the anti-inflammatory effects of Nodosin from Isodon serra, a traditional Chinese herb medicine, mouse T lymphocytes were incubated with Nodosin. In the current study, Nodosin suppressed the overproduction of the T lymphocytes; moreover, cell mitosis cycle was modulated by interfering with DNA replication in G1 stages via inhibition of IL-2 cytokine secretion at the mRNA level by Nodosin. Interestingly, Xylene-induced mouse tumescence model results suggested Nodosin depressed the murine ear-swelling extent and the level of IL-2 in the blood serum. Finally, Nodosin possessed significant anti-inflammatory effects and is a potential candidate for further clinical trial.

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A longitudinal study of the relationship between psychological distress and recurrence of upper respiratory tract infections in chronic fatigue syndrome

British Journal of Health Psychology ◽

10.1348/135910706x171469 ◽

2008 ◽

Vol 13 (1) ◽

pp. 177-186 ◽

Cited By ~ 19

Author(s):

Susan Faulkner ◽

Andrew Smith

Keyword(s):

Psychological Distress ◽

Longitudinal Study ◽

Respiratory Tract Infections ◽

Chronic Fatigue ◽

Upper Respiratory Tract Infections ◽

Upper Respiratory Tract ◽

Fatigue Syndrome ◽

Upper Respiratory ◽

Tract Infections ◽

The Relationship

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“Post-COVID syndrome”: The focus is on musculoskeletal pain

Rheumatology Science and Practice ◽

10.47360/1995-4484-2021-255-262 ◽

2021 ◽

Vol 59 (3) ◽

pp. 255-262

Author(s):

A. E. Karateev ◽

V. N. Amirdzhanova ◽

E. L. Nasonov ◽

A. M. Lila ◽

L. I. Alekseeva ◽

...

Keyword(s):

Chronic Pain ◽

Chronic Fatigue ◽

Organ Damage ◽

Modern Medicine ◽

Multiple Organ ◽

Functional Disorders ◽

Fatigue Syndrome ◽

Urgent Task ◽

Long Time ◽

Autoimmune Processes

Combating the consequences of COVID-19, a disease caused by the new coronavirus infection SARS-CoV-2, is a serious and very urgent task facing modern medicine. COVID-19 often has a severe course and is accompanied by multiple organ damage, systemic immune inflammation, coagulopathy, neuroendocrine and metabolic disorders. Even with a relatively favorable course, the consequences of SARS-CoV-2 infection can be degenerative changes in many organs (pulmonary fibrosis, cardiosclerosis), various functional and psychoemotional disorders. As a result, in 10–50% of patients, various unpleasant symptoms persist for a long time after the acute manifestations of COVID-19 subside and the virus is eliminated. This pathology is referred to as “post-COVID syndrome” (PCS). The main elements of PCS are chronic pain, fatigue, and psychoemotional problems. Functional disorders, autoimmune processes, and severe psychological distress after COVID-19 can cause the development and exacerbation of diseases characterized by chronic pain and fatigue, such as fibromyalgia and chronic fatigue syndrome. Therapy and prevention of PCS include correction of functional disorders, pain control, and consistent physical, psychological, and social rehabilitation.

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Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2021.673217 ◽

2021 ◽

Vol 15 ◽

Author(s):

Adonis Sfera ◽

Carolina Osorio ◽

Carlos M. Zapata Martín del Campo ◽

Shaniah Pereida ◽

Steve Maurer ◽

...

Keyword(s):

Chronic Fatigue Syndrome ◽

Viral Infections ◽

Life Quality ◽

Chronic Fatigue ◽

Myalgic Encephalomyelitis ◽

Unknown Etiology ◽

Host Proteins ◽

Fatigue Syndrome ◽

Long Time ◽

Sleep Abnormalities

Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.

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Chronic fatigue syndrome and susceptibility to upper respiratory tract illness

British Journal of Health Psychology ◽

10.1348/135910799168678 ◽

1999 ◽

Vol 4 (4) ◽

pp. 327-335 ◽

Cited By ~ 6

Author(s):

Andrew Smith ◽

Marie Thomas ◽

Leszek Borysiewicz ◽

Meirion Llewelyn

Keyword(s):

Chronic Fatigue Syndrome ◽

Respiratory Tract ◽

Chronic Fatigue ◽

Upper Respiratory Tract ◽

Fatigue Syndrome ◽

Respiratory Tract Illness ◽

Upper Respiratory

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Potential Implications of Mammalian Transient Receptor Potential Melastatin 7 in the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Review

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph182010708 ◽

2021 ◽

Vol 18 (20) ◽

pp. 10708

Author(s):

Stanley Du Preez ◽

Helene Cabanas ◽

Donald Staines ◽

Sonya Marshall-Gradisnik

Keyword(s):

Chronic Fatigue Syndrome ◽

Molecular Mechanisms ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Chronic Fatigue ◽

Myalgic Encephalomyelitis ◽

Potential Candidate ◽

Fatigue Syndrome ◽

Organ Systems ◽

Transient Receptor

The transient receptor potential (TRP) superfamily of ion channels is involved in the molecular mechanisms that mediate neuroimmune interactions and activities. Recent advancements in neuroimmunology have identified a role for TRP cation channels in several neuroimmune disorders including amyotropic lateral sclerosis, multiple sclerosis, and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating disorder with an obscure aetiology, hence considerable examination of its pathobiology is warranted. Dysregulation of TRP melastatin (TRPM) subfamily members and calcium signalling processes are implicated in the neurological, immunological, cardiovascular, and metabolic impairments inherent in ME/CFS. In this review, we present TRPM7 as a potential candidate in the pathomechanism of ME/CFS, as TRPM7 is increasingly recognized as a key mediator of physiological and pathophysiological mechanisms affecting neurological, immunological, cardiovascular, and metabolic processes. A focused examination of the biochemistry of TRPM7, the role of this protein in the aforementioned systems, and the potential of TRPM7 as a molecular mechanism in the pathophysiology of ME/CFS will be discussed in this review. TRPM7 is a compelling candidate to examine in the pathobiology of ME/CFS as TRPM7 fulfils several key roles in multiple organ systems, and there is a paucity of literature reporting on its role in ME/CFS.

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