Unraveling the Molecular Mechanism of Traditional Chinese Medicine: Formulas Against Acute Airway Viral Infections as Examples

Abstract

Herbal medicine, including traditional Chinese medicine (TCM), is widely used worldwide. Herbs and TCM formulas contain numerous active molecules. Basically, they are a kind of cocktail therapy. Herb-drug, herb-food, herb-herb, herb-microbiome, and herb-disease interactions are complex. There is potential for both benefit and harm, so only after understanding more of their mechanisms and clinical effects can herbal medicine and TCM be helpful to users. Many pharmacologic studies have been performed to unravel the molecular mechanisms; however, basic and clinical studies of good validity are still not enough to translate experimental results into clinical understanding and to provide tough evidence for better use of herbal medicines. There are still issues regarding the conflicting pharmacologic effects, pharmacokinetics, drug interactions, adverse and clinical effects of herbal medicine and TCM. Understanding study validation, pharmacologic effects, drug interactions, indications and clinical effects, adverse effects and limitations, can all help clinicians in providing adequate suggestions to patients. At present, it would be better to use herbs and TCM formulas according to their traditional indications matching the disease pathophysiology and their molecular mechanisms. To unravel the molecular mechanisms and understand the benefits and harms of herbal medicine and TCM, there is still much work to be done.

Keywords: alternative medicine; complementary medicine; prescription; therapy.

Figure 1

The molecular mechanism of TCM formulas against airway viral infections. Airway viruses infect the epithelium to cause tissue injury. TCM formulas of A-physicians contain several active molecules to inhibit viral replication and signal transduction of inflammatory response. Akt: Serine/threonine protein kinase B (PKB); COX: Cyclooxygenase; ERK: Extracellular signal-regulated kinase; IL: Interleukin; iNOS: Inducible nitric oxide synthases; JNK: c-Jun N-terminal kinases; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-kappa B; NO: Nitric oxide; PG: prostaglandin; PI3K: Phosphoinositide 3-kinase; PMN: Polymorphonuclear neutrophils; TNF: Tumor necrotic factor.

Figure 2

Molecular mechanism of Ge-Gen-Tang against airway viral infections. Airway viruses infect the epithelium to cause tissue injury. Ge-Gen-Tang contains several active molecules to inhibit viral replication and signal transduction of inflammatory response. Akt: Serine/threonine protein kinase B (PKB); COX: Cyclooxygenase; ERK: Extracellular signal-regulated kinase; IL: Interleukin; iNOS: inducible Nitric oxide synthases; JNK: c-Jun N-terminal kinases; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-kappa B; NO: Nitric oxide; PG: Prostaglandin; PI3K: Phosphoinositide 3-kinase; PMN: Polymorphonuclear neutrophils; TNF: Tumor necrotic factor.

Figure 3

Molecular mechanism of Ma-Huang-Tang against airway viral infections. Airway viruses infect the epithelium to cause tissue injury. Ma-Huang-Tang contains several active molecules to inhibit viral replication and signal transduction of inflammatory response. Akt: Serine/threonine protein kinase B (PKB); COX: Cyclooxygenase; ERK: Extracellular signal-regulated kinase; IL: interleukin; iNOS: Inducible nitric oxide synthases; JNK: c-Jun N-terminal kinases; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-kappa B; NO: Nitric oxide; PG: Prostaglandin; PI3K: Phosphoinositide 3-kinase; PMN: Polymorphonuclear neutrophils; TNF: Tumor necrotic factor.

Figure 4

Molecular mechanism of Ma-Xing-Gan-Shi-Tang against airway viral infections. Airway viruses infect the epithelium to cause tissue injury. Ma-Xing-Gan-Shi-Tang contains several active molecules to inhibit viral replication and signal transduction of inflammatory response. Akt: Serine/threonine protein kinase B (PKB); COX: Cyclooxygenase; ERK: Extracellular signal-regulated kinase; IL: Interleukin; iNOS: Inducible nitric oxide synthases; JNK: c-Jun N-terminal kinases; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-kappa B; NO: Nitric oxide; PG: Prostaglandin; PI3K: Phosphoinositide 3-kinase; PMN: Polymorphonuclear neutrophils; TNF: Tumor necrotic factor.

Figure 5

Molecular mechanism of Xiao-Qing-Long-Tang against airway viral infections. Airway viruses infect the epithelium to cause tissue injury. Xiao-Qing-Long-Tang contains several active molecules to inhibit viral replication and signal transduction of inflammatory response. Akt: Serine/threonine protein kinase B (PKB); COX: Cyclooxygenase; ERK: Extracellular signal-regulated kinase; IL: Interleukin; iNOS: Inducible nitric oxide synthases; JNK: c-Jun N-terminal kinases; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-kappa B; NO: Nitric oxide; PG: Prostaglandin; PI3K: Phosphoinositide 3-kinase; PMN: Polymorphonuclear neutrophils; TNF: Tumor necrotic factor.

Figure 6

Molecular mechanism of Ye-Gan-Ma-Huang-Tang against airway viral infections. Airway viruses infect the epithelium to cause tissue injury. Ye-Gan-Ma-Huang-Tang contains several active molecules to inhibit viral replication and signal transduction of inflammatory response. Akt: Serine/threonine protein kinase B (PKB); COX: Cyclooxygenase; ERK: Extracellular signal-regulated kinase; IL: interleukin; iNOS: Inducible nitric oxide synthases; JNK: c-Jun N-terminal kinases; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear factor-kappa B; NO: Nitric oxide; PG: prostaglandin; PI3K: Phosphoinositide 3-kinase; PMN: Polymorphonuclear neutrophils; TNF: Tumor necrotic factor.