A review on the molecular basis underlying the protective effects of Andrographis paniculata and andrographolide against myocardial injury.
Sok Kuan WongKok-Yong ChinSoelaiman Ima-NirwanaPublished in: Drug design, development and therapy (2021)
Andrographolide is the major compound found in the medicinal plant, Andrographis paniculata (Burm.f.) Nees, which accounts for its medicinal properties. Both the plant extract and compound have been reported to exhibit potential cardiovascular activities. This review summarises related studies describing the biological activities and target mechanisms of A. paniculata and andrographolide in vivo and in vitro. The current evidence unambiguously indicated the protective effects provided by A. paniculata and andrographolide administration against myocardial injury. The intervention ameliorates the symptoms of myocardial injury by interfering with the inductive phase of a) inflammatory response mediated by nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3) signalling molecules; b) oxidative stress via activation of nuclear factor erythroid 2-related factor (Nrf-2) and reduction of enzymes responsible for generating reactive oxygen and nitrogen species; c) intrinsic and extrinsic mechanisms in apoptosis regulated by upstream insulin-like growth factor-1 receptor (IGF-1R) and peroxisome proliferator-activated receptor-alpha (PPAR-α); d) profibrotic growth factors thus reducing cardiac fibrosis, improving endothelial function and fibrinolytic function. In conclusion, A. paniculata and andrographolide possess therapeutic potential in the management of myocardial injury, which requires further validation in human clinical trials.
Keyphrases
- nuclear factor
- oxidative stress
- protein kinase
- toll like receptor
- inflammatory response
- clinical trial
- signaling pathway
- induced apoptosis
- cell proliferation
- randomized controlled trial
- endothelial cells
- left ventricular
- pi k akt
- ischemia reperfusion injury
- diabetic rats
- lps induced
- endoplasmic reticulum stress
- type diabetes
- immune response
- mouse model
- cell cycle arrest
- cell death
- cell wall
- insulin resistance
- anti inflammatory
- adipose tissue
- study protocol
- climate change
- heat shock protein
- physical activity