A. paniculata have shown a broad range of pharmacological effects such as anti-viral, antibacterial, prevention of common cold, anti-diarrheal, support healthy blood glucose, and support healthy inflammatory response.
It is know as the “king of bitters” due to its bitter flavor profile. Andrographolide, an active ingredient in Andrographis, has been shown to be responsible for the herb’s inflammatory modulating actions.
ParActin® Group Showed Significant Diminishing In:
In another clinical published on Innovative Rheumatology Jan 2013, 8 patients with various rheumatoid conditions were given 300mg of ParActin® daily for 3 ½ years. Treatment with ParActin® showed significant improvement in number of swollen joints, total grade of swollen joint, total grade of tender joints, and improvement in Quality of Life. In addition, we are seeing significant reduction in Rheumatoid Factor, Eryhrocytes Sedimentation Rate, Pain, and C-Reactive Protein.
ParActin® significantly reduced the RF value from 110 to 70 mg/dl. The placebo group, did not experience any significant change in RF value.
Innovative Rheumatology Jan 2013:
In another clinical published on Innovative Rheumatology Jan 2013, 8 patients with various rheumatoid conditions were given 300mg of ParActin® daily for 4 years.
Treatment with ParActin® showed significant improvement in number of swollen joints, total grade of swollen joint, total grade of tender joints, and improvement in Quality of Life. In addition, we are seeing significant reduction in Rheumatoid Factor, Erythrocytes Sedimentation Rate, and C-Reactive Protein.
Serum immunological parameters of inflammation were reduced progressively during 48 month of ParActin® treatment. After 24 months the treatment with Paractin®, 6 patients were administered only with ParActin® as monotherapy. All patients are showing full tolerability, no remission of clinical and serological inflammatory parameters.
Significant Reduction in Rheumatoid Factors and C-Reactive Protein
Reduction in Fatigue & Pain
ParActin® Increase Osteoblast
Via COX-2 mRNA Expression
ParActin® Has Mineralizing Effect,
Increasing Calcium Deposits In TheBones
ParActin® Reduces Muscle Damage and Lowered Serum Creatine Kinase
Administration of ParActin® reduced necrosis, and cumulative muscle damage compared with vehicle-treated mdx mice. Concordantly, serum CK levels were decreased in ParActin® treated mdx mice compared with control mdx mice, with an approximately 50% recovery score.
ParActin® Reduces Fibrosis: Fibronectin and Collagen III
Development of fibrosis in is characterized by an increase in extracellular matrix compounds such as fibronectin and several types of collagen. ParActin® treatment decreased fibronectin and collagen III protein levels. ParActin® treated mice exhibited less severe muscular dystrophy, performed better in an exercise endurance test, and had improved muscle strength compared to untreated mdx mice.
ParActin® Reduces Pro-Fibrotic Factor: TGF-b, b, b, b, CTGF, and Collagen Type I
ParActin® treatment reduced TGF-β, an important pro-fibrotic factor in mdx skeletal muscle. In addition, Connective tissue growth factor (CTGF) and collagen type I, two downstream pro-fibrotic factors in dystrophic skeletal muscle were also reduced by ParActin® treatment.
ParActin® Improves Skeletal Muscle Strength and Exercise Performance
ParActin®-treated mdx mice showed an enhanced exercise performance, significant increase in the generation of isometric force, and higher strength in the TA muscle. This is evidenced by a significant decrease in the number of detentions in the treadmill running protocol, with recovery score of 45.5%.
ParActin® Reduces Tau Hyperphosphorylation
Tau protein stabilizes microtubules and is abundantly present in brain. Beta amyloid induces the occurrence of phospho-epitopes in tau protein associated with neuronal damage. When Tau protein is defective, they no longer stabilizes microtubules properly and can result in dementia such as Alzheimer. ParActin® prevents tau hyperphosphorylation, increases field excitatory postsynaptic potentials, and inhibits long-term depression (LTD) via the inhibition of the glycogen synthase kinase-3β.
ParActin® Activates Wnt Signaling By Inhibition of GSK-3β & Stimulates Neurogenesis
Glycogen synthase kinase-3β is an enzyme that regulates Wnt signaling pathway, gene transcription, and neuronal cell function. The Wnt/β-catenin signaling pathway is essential in the nervous system and participates in the neural tube formation and midbrain development. Blocked Wnt pathway caused reduced neurogenesis and impaired learning and memory function. ParActin® activates Wnt signaling pathway by a mechanism that bypasses the Wnt receptor and involves inhibition of GSK-3β. In silico analyses ParActin® directly inhibits GSK-3β by competing at the substrate binding site.
In vivo research showed that treatment of 2 month-old wild-type mice treated with ParActin® for 4 weeks strongly induces cell proliferation and the generation of newborn neurons in the dentate gyrus, increases density of immature neurons, increases percentage of the granular cell layer, more complex morphology, and induces development of newborn neurons.
HP Ingredients offers custom formulations and private labeling services to manufacturers. HPI’s innovation in formulations is accomplished by combining our trademarked ingredients with other clinically tested, well-researched nutraceuticals.