Aralia chinensis Extract

oleanolic acid ursolic acid Olea europaea Extract

• Protect liver and depress enzyme£¬ Anti-inflammation, Diuretic,Anti-cancer
  Two triterpene acids, oleanolic acid (OA) and ursolic acid (UA), purified components from several Botanical drugs with known antitumor activity such as, were examined for their ability and possible pathway on inhibiting the tumor growth of hepG2 cells. Cells were treated with OA and UA with doses of 100 and 200 ug/ml for 12, 24 and 36 hrs, respectively. The changes of DNA fragmentation, apoptotic bodies, DNA synthesis and the expression of cell cycle related genes were investigated after various treatments. Decrease of DNA synthesis in cells treated with both OA and UA was obviously observed at these doses for 24 and 36 hrs by using BrdU staining method. Total RNA were purified with RNA Zol B reagent and the first stranded cDNA were synthesized by AMV transcriptase. Semiquantitation of the cDNA was performed by primer dropping method. Both mRNA and protein of the CDK inhibitor of INK4 family which specifically inhibits CDK4/6 activity and then reduces the phosphorylation of RB, p-15INK4b, in hepG2 cells were greatly induced by OA and UA. However, the expression of another member in this family, p-16INK4a, was not significantly induced. Other CDK inhibitors such as p-21CIP, p-27KIP and cell cycle related genes were not induced after various OA and UA treatments. The DNA fragmentation and apoptotic bodies were also found in this study with both the time- and dose-dependent phenomena. These results suggested that the apoptosis induced by OA and UA might be partially mediated through PKC pathway and associated with p-15INK4b gene induction.
• Ursolic acid (UA) and oleanolic acid (OA), isolated from Glechoma hederacea, inhibited Epstein-Barr virus activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin. The inhibitory effects were evaluated for 20 weeks. Continuous application of UA and OA (41 nmol of each) before TPA-treatment (4.1 nmol) delayed the formation of papillomas in mouse skin and reduced the rate (%) of papilloma bearing mice. Both UA and OA exhibited remarkable inhibitory activity against tumor promotion, which is comparable to the known tumor inhibitor, retinoic acid (RA). Compared to either RA or OA, ursolic acid inhibited tumors more effectively after a single application before initial TPA-treatment. This suggests that the role of tumor inhibition by UA differs from that of either RA or OA. It is suggested that pretreatment of skin with UA may inhibit the first dramatic cellular event in tumor promotion caused by TPA1.
• Ursolic acid and its isomer, oleanolic acid have been recommended for skin cancer therapy in Japan2. Topical cosmetic preparations containing ursolic acid/oleanolic acid have been patented in Japan for the prevention of topical skin cancer7. An ursolic acid/oleanolic acid ointment inhibited 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin cancer in mice. Reportedly, 0% and 3% of mice developed cancer in 15 weeks and 30 weeks, respectively compared to 50% and 90% for the control mice7.
  Ursolic acid treatment improves the health of skin and hair. Ursolic acid and its derivatives form oil-resistant barriers on the skin and hair as they do in the waxy coating of fruits3. Ursolic acid has been used to treat photoaged skin because it prevents and improves the appearance of wrinkles and age spots by restoring the skin¡¯s collagen bundle structures and its elasticity4. Concentrations of ursolic acid ranging from 0.01 to 50 mg have been reported for inclusion in skin treatment preparations5-6.