Apocynin is well known as a NADPH oxidase inhibitor with anti-inflammatory effects including due to the suppression of the generation of ROS.
Apocynin improves the function of active stem cells, re-awakens dormant stem cells, and has potent immune-regulatory properties. By strengthening the immune system, Apocynin also helps the body clear away “zombie” cells.
Research with Apocynin has shown benefit in a broad range of chronic health conditions such as:
- Prevent the progression of atherosclerosis, suppressed the Ox-LDL , cytokines, and macrophages (3)
- Ameliorated colonic inflammation (4)
- Can partially reverse the inflammation in chronic inflammatory joint diseases like osteoarthritis or rheumatoid arthritis (5)
- Exhibits COX inhibitory effects similar to ibuprofen (5)
- Significantly attenuates hepatic oxidative stress and inflammation induced by alcoholic steatohepatitis (fatty liver) (6)
The powerful anti-inflammatory effects of Apocynin are also beneficial for the skin (1,2). In a new paper published in Nature, a research team found that a collagen protein called COL17A1 plays a key role in maintaining youthful skin. Declining levels of this protein over time cause our skin to develop wrinkles, sag, and lose its elasticity. Apocynin was able to restore levels of COL17A1 and repair damaged skin, leading the scientists to say that it may be possible to reverse our skin’s timeline at the cellular level.
NADPH oxidases produce ROS
Oxidative stress is a common underlying mechanism for multiple diseases such as cardiovascular diseases, and neurodegenerative disorders (7).
NADPH oxidases produce reactive oxygen species (ROS) as their primary and sole function. They are widely distributed throughout different tissues and organs and are suggested to play important roles in multiple diseases associated with oxidative stress.
Targeting the sources of ROS is now recognized as a more effective strategy rather than trying to scavenge ROS after they have been produced.
Therefore, NADPH oxidases are prime candidates for the treatment of many diseases (7).
ROS increases inflammation and consumes NAD+
NADPH oxidases increase ROS and inflammation.
Inflammation leads to increased CD38 which causes NAD+ decline and subsequent mitochondrial dysfunction (8).
NADPH oxidase inhibitors such as Apocynin are a powerful therapy for restoring NAD+ levels.
Research on Apocynin
we identified two chemicals—Y27632 and apocynin— that induced COL17A1 expression in keratinocytes.
Application of these drugs to full-thickness skin wounds significantly promoted wound repair
Small molecules that stabilize COL17A1 promote skin wound healing, and may therefore be beneficial for organ integrity, regeneration and the reduction of ageing.
Recently, Apocynin (APO) has emerged as a bioactive phytochemical with potent antioxidant and anti-inflammatory properties.
In the current research, we focused on exploiting the tremendous benefits of APO, a specific NADPH-oxidase inhibitor, and CAS, a protein film former, as natural biocomponents to develop novel anti-inflammatory topical film.
The film can be applied in case of pressure ulcer, wounds, and burns. In summary, this study highlights the prospective topical application of CAS film loaded with APO for management of inflammatory disorders.
Production of reactive oxygen species (ROS) and other proinflammatory substances by macrophages plays an important role in atherogenesis. Apocynin (4-hydroxy-3-methoxy-acetophenone), which is well known as a NADPH oxidase inhibitor, has anti-inflammatory effects including suppression of the generation of ROS.
In conclusion, we have demonstrated that apocynin suppressed ROS generation in atherosclerotic lesions and prevented the progression of atherosclerosis. These results suggested that apocynin would be a potential therapeutic material to prevent the progression of atherosclerosis.
Apocynin, a constituent of Picrorhiza kurroa, successfully inhibits NADPH oxidase and shows promise as an anti-inflammatory drug. Now, we report anti-inflammatory effects of apocynin in an experimental colitis model
Apocynin reduced the colitis induced in mice by administration of 5 % dextran sulfate sodium during 7 days.
Treatment with apocynin and rutin ameliorated the course of colonic inflammation
These results are promising for further experimental studies on treating gastrointestinal diseases and on the potential protective effects of apocynin.
Apocynin, an inhibitor of NADPH-oxidase, is known to partially reverse the inflammation-mediated cartilage proteoglycan synthesis in chondrocytes.
Apocynin dose-dependently reversed the inhibition of proteoglycan synthesis in articular cartilage of the arthritic joint.
Apocynin significantly decreased the zymosan-induced ear swelling at 1, 2 and 4 h (hours)
oral administration of apocynin can partially reverse the inflammation-induced inhibition of cartilage proteoglycan synthesis
oral administration of apocynin has COX inhibitory effects similar to the non-steroidal anti-inflammatory drug (NSAID) ibuprofen.
apocynin might be of potential use during the treatment of chronic inflammatory joint diseases like osteoarthritis or rheumatoid arthritis.
Apocynin is a widely used antioxidant in both basic and clinical research.
Co-treatment of apocynin alleviated the hepatic injury and biochemical parameters induced by alcoholic steatohepatitis.
In conclusion, addition of apocynin significantly attenuates hepatic oxidative stress and inflammation induced by alcoholic steatohepatitis. This effect is partly through the inhibition of the RAS system.
Oxidative stress increases with age in human skin, leading to a PARP mediated decline in NAD+ levels.
It is generally accepted that the mitochondria (the site of oxidative phosphorylation and ATP generation) is the major source of ROS production.
Previous studies have shown that age-associated mitochondrial dysfunction increases with age. This can severely compromise the efficiency of the ETC, resulting further ROS generation.
Impairment in mitochondrial function and the consequent reduction in ATP- production may explain both the pro-oxidant shift and energy deficit in aging.
An extensive body of evidence has demonstrated the importance of oxidative stress in its contribution to the aging process. This study reports for the first time a link between oxidative stress and PARP activity, aging and a decline in NAD+ levels, in human tissue.
Nicotinamide Adenine Dinucleotide (NAD) levels decrease during aging, and are involved in age-related metabolic decline.
Here we demonstrate that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of SIRT3 activity.
We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.