ParActin® is a patented extract of Andrographis paniculata, standardized to andrographolide, 14 deoxyadngrographolide, and neo-andrographolide.
Muscles are susceptible to damage, just like other body tissues. Trauma, infections, certain medications or even strenuous exercise can cause varying degrees of muscle injury. “No pain, no gain.” Well, if you’re over the age of 40, no pain is actually a good thing. If you find yourself in the discomfort zone, your body may be trying to tell you something. Being over 40 means that our bodies have had more years of wear and tear and have become susceptible to the repetitive stress that can cause injury. While you may feel strong and ready to take on any physical activity, your bones, muscles and joints could be more delicate than you realize. As we age, our musculoskeletal system—bones, joints, tendons, ligaments and muscles—changes in that we gradually lose muscle mass and the connective tissues—tendons, ligaments, cartilage and other support structures—lose some of the flexibility and resilience that is present when we are young. And in addition to the loss of elasticity and resilience, low bone density conditions such as osteopenia and osteoporosis can further complicate matters.
Skeletal muscle injuries constitute the majority of sports-related injuries. Injured skeletal muscle undergoes the healing phases of degeneration, inflammation, regeneration, and
fibrosis. Your body heals damaged tissue fibers by laying down new soft tissue fibers as part of the secondary phase of the inflammatory process. This occurs in bone, muscle, tendon, ligament, joint capsules and cartilage. Healthy new fibers are essential to healing and pain relief as they replace the torn and damaged ones.
In a pivotal study published in Skeletal Muscle 2014, mdx mice (mice studied particularly for muscle degeneration and regeneration) were treated with ParActin® for 3 months. ParActin® was shown to promote muscle health and recovery, making it quite ideal for those engaged in regular fitness routines, hard labor, or athletic participation. Three positive effects were observed in this study, as follows:
- ParActin® reduces inflammation in the skeletal muscle via inhibition of NF-kB
Prostaglandins (PGEs) have been identified and implicated as major factors in tissue inflammation. Many PGEs are synthesized by cyclooxygenase enzyme and are largely produced during the inflammatory phase after muscle injury. Aspirin and other NSAIDs inhibit prostaglandin synthesis, and are typically recommended be taken in the first few days after injury to limit inflammation and pain. However, long term use of these NSAIDs may cause stomach discomfort. Multiple studies have proven the effectiveness of selective COX-2 inhibitors in the reduction of joint and muscle pain with gastrointestinal safety. Supplementation with ParActin® reduced the number of nuclei positive for NF-κB in the Paractin® group, reduced COX-2 enzyme, which in turns reduce the PGEs concentrations that causes pain and inflammation.
- ParActin® Reduces Fibrosis and Pro-Fibrotic Factor
Transforming growth factor type beta (TGF-β1) and connective tissue growth factor (CTGF) have been shown to inhibit skeletal muscle regenerative processes. They replace connective tissue scar that is composed of fibronectin, as well as type I and type III collagen. This fibrotic tissue provides early support for damage skeletal muscle. Unfortunately, these new fibers do not arrange in the same direction that the original fibers were oriented, resulting in a scar formation (fibrosis) in the injured muscle. Fibrosis often causes stiffness, abnormal joint function, nerve pain, and restricts the regenerative process. Recurring injury and loss of muscle strength after muscle injuries may be attributable to TGF-ß1–induced fibrosis within the muscle.
ParActin® administration significantly decreased fibronectin, collagen I, and collagen III levels.
In addition, ParActin® treatment reduced TGF-β1 and CTGF, two pro-fibrotic factors that contribute to fibrosis and prevent proper muscle regeneration process. By Blocking TGF-ß1 and thus reducing scar tissue, ParActin® helps to facilitate improved muscle functional recovery.
- ParActin® Reduces Muscle Damage and Lowered Serum Creatine Kinase
Strenuous exercise and overtraining can lead to structural damage to muscle cells which triggers white blood cells to increase following the induced muscle soreness, leading to the inflammatory response. This has been noted especially in marathon runners whose muscle fibers revealed remarkable damage after both training and marathon competition. The muscle damage causes calcium to leak out of the muscle, which further leads to the activation of enzymes that break down cellular proteins in the muscle. These proteins then cause an inflammatory response by the immune system which then leads to swelling (water retention at the site of injury) and pain.
In one study, administration of ParActin® reduced necrosis, and cumulative muscle damage compared with control mdx mice.
Creatine kinase (CK) is a type of enzyme found within your muscles, including heart and brain. Serum CK indicates the overall health of the muscles within the body and if a serum CK test shows elevated levels, this is an indicator of strain on the muscles that may have been caused by simply heavy exercise or something as serious as a heart attack. Inflammation of muscle and other skeletal muscle damage are associated with an elevated creatine kinase level.
- ParActin® Improves Skeletal Muscle Strength and Exercise Performance
ParActin®-administrated mdx mice showed improved skeletal muscle strength and enhanced exercise performance. ParActin®-administrated mdx mice showed significant increase in the generation of isometric force; increase twitch and tetanic force in the Tibialis anterior (TA) muscle (in front of the shin); and significant decrease in the number of fall back in the treadmill running protocol, with recovery score of 45.5%.
The author concludes that the supplement group exhibited less severe muscular dystrophy, performed better in an exercise endurance test, and had improved muscle strength compared to control mdx mice.
