METHODS: The active compounds in cocoa pod extracts (CPE) were screened using liquid chromatography-mass spectrometry (LC-MS). Fibroblast cells were used to determine the effective concentration of CPE to maintain the viability for at least 50% of the cells (EC50 ). The gel was tested by 12 panelists to determine the efficacy of CPE in gel form using Visioscan to reduce skin wrinkles and improve skin condition.
RESULTS: CPE was detected to contain malic acid, procyanidin B1, rosmarinic acid, procyanidin C1, apigenin, and ellagic acid, all of which may contribute to functional cosmetic properties of CPE. The EC50 value of cocoa pod extracts was used to calculate the amount of CPE to be incorporated into gel so that the formulated product could reach an effective concentration of extract while being nonintoxicant to the skin cell. The results showed that CPE is potential ingredient to reduce wrinkles. Skin wrinkles reduced at 6.38 ± 1.23% with the application of the CPE gel within 3 weeks and significantly improved further (12.39 ± 1.59%) after 5 weeks. The skin hydration increased (3.181 ± 1.06%) after 3 weeks of the CPE gel application.
CONCLUSION: Flavonoid compounds in CPE contributed to the functional cosmetic properties of CPE. The CPE which is nontoxic to skin cells help to reduce wrinkles on skin after 3 weeks of application. CPE can be used as the active ingredients in antiwrinkle products, and prolonged application may result in significant visual changes to the naked eyes.
OBJECTIVE: To determine the clinical characteristics, culprit drugs and outcome of patients with AGEP.
METHODS: A retrospective note review of all AGEP patients seen from 2001-2015.
RESULTS: Among 21 AGEP patients, 76% were Malays, 9.5% Chinese, 9.5% Indians, and 5% Iban. Sixteen were females and 5 were males. Median age of patients was 40 years (IQR: 26). The main culprit drug was amoxicillin (10 cases), followed by cloxacillin (three cases), phenytoin (two cases) and one case each of carbamazepine, sulphasalazine, allopurinol, cephalexin, ceftriaxone, celecoxib and herbal product. The median time from drug initiation to onset of AGEP was 3 days (IQR: 5.5). Fever was documented in 52.4 %, mucosal involvement 9.5%, purpura 4.7% and blisters 4.7%. Neutrophilia was observed in 63.6% of patients and eosinophilia in 28.5%. While most patients required admission (67%), all achieved complete recovery within 15 days without any sequela.
CONCLUSIONS: AGEP predominantly affects Malay females in this study. The most common culprit drug was amoxicillin. Our patients exhibited the classic clinical manifestations of AGEP and confirmed the generally benign nature of this reaction upon drug withdrawal. Although the overall prognosis is good, prompt diagnosis of AGEP is important because drug withdrawal is the mainstay therapy.
METHODS: Mice were initiated with single dose of 7,12-dimethylbenz[α]anthracene (DMBA) (390 nmol/100 μL) followed by, in subsequent week, repeated promotion (twice weekly; 22 weeks) with 12-O-tetradecanoylphorbol-13-acetate (TPA) (1.7 nmol/100 μL). Annonacin (85 nM) and curcumin (10 mg/kg; reference) were, respectively, applied topically to DMBA/TPA-induced mice 30 min before each TPA application for 22 weeks. Upon termination, histopathological examination of skin, liver and kidney as well as genes and proteins expression analysis were conducted to elucidate the potential mechanism of annonacin.
RESULTS: With comparison to the carcinogen control, Annonacin significantly increased the tumor latency period and reduced the tumor incidence, tumor burden and tumor volume, respectively. In addition, it also suppressed tumorigenesis manifested by significant reduction of hyperkeratosis, dermal papillae and number of keratin pearls on skin tissues. Annonacin also appeared to be non-toxic to liver and kidney. Significant modulation of both AKT, ERK, mTOR, p38, PTEN and Src genes and proteins were also observed in annonacin-targeted signaling pathway(s) against tumorigenesis.
CONCLUSIONS: Collectively, results of this study indicate that annonacin is a potential therapeutic compound targeting tumor promoting stage in skin tumorigenesis by modulating multiple gene and protein in cancer signaling pathways without apparent toxicity.