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Capsicum annuum Capsaicin (8-methyl-N-vanillyl-6-nonenamide) comes from chili peppers and gives them their heat. Capsaicin has a lot to offer, and its analgesic properties are at the top of the list. Capsaicin is used to help relieve pain. Capsaicin works by first stimulating and then decreasing the intensity of pain signals in the body. Capsaicin stimulates the release of a compound believed to be involved in communicating pain between the nerves in the spinal cord and other parts of the body.
Zingiber officinale : Zingiber officinale commonly known as ginger, has been widely used traditionally for a variety of medicinal purposes, one of which is for the treatment of pain. Seven published articles, reporting a total of eight trials (481 participants), were included in the review. Six trials (two for osteoarthritis, one for dysmenorrhea, and three for experimentally induced acute muscle pain) found that the use of Z. officinale reduced subjective pain reports.
Rheum emodi : Rheum emodi wall has been reported to possess protective effect in many inflammatory diseases and oxidative stress-related injuries. The most abundant stilbenoid piceatannol-4-O-β-D-glucopyranoside (PICG) and its aglycon piceatannol (PICE) were isolated from R. emodi rhizome. Using well-accepted antioxidant chemicals as reference, antioxidant activity of these stilbenoids was examined by measuring DPPH and superoxide anion radical scavenging, ferric reducing power, and inhibition of lipid peroxidation in vitro.

Mechanism of Action:
Capsaicin activates afferent nociceptive neurons and evokes sensation ranging from hotness to burning. Its analgesic properties are mediated by the depletion of substance -P that leads to the desensitization of small afferent sensory neurons. Capsaicin binds to a specific nerve membrane receptor, the Transient Receptor potential vanilloid 1 receptor (previously known as vanilloid receptor.VR1). The binding of capsaicin to TRPV1 receptor in small fiber sensory afferent nerve ending activation the receptor and this leads to an influx of calcium and the release of inflammatory neuropeptides. This mediates the pungent properties of capsaicin and limits its leads to analgesia. In addition there may be degeneration of nociceptive fibers. Capsaicin down regulates these voltage activated calcium channels by dephosphorylation (via a calcium dependent activation of calcineurin). This is the mechanism by which capsaicin reduces inflammatory hyperalgesia.