Figure 1
Risk factors of cardiovascular diseases (CVDs) and inflammation. Hypertension and hyperlipidemia are the risk factors of CVDs and induce inflammation in the heart and vessels. Unhealthy diet along with genetic factors lead to the development of hypertension and hyperlipidemia and induce inflammation. Smoking and infection also induce inflammation and lead to CVDs.
Figure 2
Immunoglobulin free light chains (FLCs) as biomarkers of inflammatory diseases. Risk factors of noncommunicable diseases (NCDs) such as CVDs and diabetes activate nuclear factor kappa B (NF-κB), which regulates the transcription of immunoglobulin free light chain κ in the immunoglobulin-producing B cells and plasma cells and the production of many inflammatory molecules, leading to inflammation. Thus, FLCs were proposed to be biomarkers of NF-κB activation and inflammation.
Figure 3
FLCs as possible predictive biomarkers of longevity. Sequential measurements of FLCs before and after the intervention of lifestyle changes (diet, exercise, etc.) or intake of supplements or drugs could predict their benefit for the longevity.
Figure 4
Antiviral effects of Pycnogenol (PYC) on encephalomyocarditis viral (EMCV) infection in mice. (A) The amount of plaque forming units in the hearts of mice after PYC oral administration (1 mg/kg and 10 mg/kg) and in control mice. (B) Expression levels of plasma pro-inflammatory cytokine TNF-α in control mice and in mice after PYC oral administration (10 mg/kg and 100 mg/kg). (C) Expression levels of plasma mast cell–related tryptase mMCP-6 in control mice and in mice after PYC oral administration (10 mg/kg and 100 mg/kg). Reproduced from Matsumori et al. [70] with permission of Elsevier.
Figure 5
The effect of PYC on hepatitis B virus in humans. (A) Copies of hepatitis B virus DNA per mL in the blood of patients after PYC or placebo administration. (B) Hepatic serum ALT enzyme concentration (U/L) in patients after PYC or placebo administration.
Figure 6
Potential mechanisms of PYC on heart failure. PYC may prevent heart failure by inhibiting inflammation by multiple pathways such as antiviral effects and inhibiting activation of NF-κB and mast cells.