Extracts of placenta serve as a potent wound healer since ancient times. Use of placenta in traditional Chinese medicine has been reported for more than 5000 years as a general tonic against headache, insomnia and disability. Various extracts of placenta have been prepared, yet until date, only an aqueous extract of placenta has been shown to be of immense therapeutic value particularly in wound healing including chronic non-healing wounds. Composition of the extracts depends on the method of its preparation. Since the indigenous extract of human placenta is prepared under high temperature and pressure, the extract contains macromolecules in degraded forms such as carried over amino acids, peptides, proteins, polynucleotides, lipids and other bioorganic compounds. In this review, clinical efficacy of aqueous extract of human placenta and the biochemical characterization of its indigenous preparation has been described.

Inflammation is a dynamic response of the vascularized tissue to an injury. It is characterized by increase in blood flow to the tissue causing Increase in temperature, Redness, Swelling, and Pain It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. In the absence of inflammation, wounds and infections would never heal and progressive destruction of the tissue would compromise the survival of the organism. Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues. A cascade of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells which are present at the site of inflammation and is characterised by simultaneous destruction and healing of the tissue from the inflammatory process. Notably, chronic inflammation has long been linked to both rheumatoid arthritis and osteoarthritis. Now, there’s emerging research that also links chronic inflammation to allergies, asthma, Alzheimer’s disease, cancer, diabetes, digestive disorders, heart disease, hormonal imbalances and osteoporosis. The inappropriate inflammation can be treated with various steroidal as well as non-steroidal anti-inflammatory drugs (NSAIDs). However, there is still need for a proper anti-inflammatory drug, as the existing ones have various side effects and are not very effective. Interestingly, a few reports have indicated that Placentrex, produced by M/s Albert David Ltd, exhibit anti-inflammatory activity (Sur et al., 2003; Banerjee et al., 1992). However, still there is no clear evidence on that, nor there is any detailed molecular study. Our objective here is to examine the anti-inflammatory activity of Placentrex in details using a cell culture model system. Our goal is to elucidate the molecular mechanism of the anti-inflammatory activity of Placentrex. We will also identify and characterize the factor (s) present in Placentrex responsible for this activity.

The drug Placentrex is found to be wonderfully efficacious against Wound healing and is a thoroughly recommended product by physicians in many Wound-healing cases. During the whole process, cell migration appears to be the rate-determining step and is a prerequisite for wound healing (Ridley et al., 2003). Therefore, our main objective is to study the effect of Placentrex on cell migration, which leads to wound healing and to find out the active principle of Placentrex, which causes wound healing. Previously Dr. Rahul Gupta at Albert David Ltd, has shown that the amino acid Glutamate (Glu) present in Plx can induce cell migration in human neutrophils (Rahul Gupta and D. J. Chattopadhyay, 2008). He further found that a particular phospholipid fraction present in Plx also has the same ability. Currently, We are extending this observation to figure out what is (are) the phospholipid factor (s) that induces cell migration. We will also perform experiments addressing the mechanism of phospholipid-mediated cell migration stimulation.