@article {1919, title = {In Silico Study of Naringenin as Melanogenesis Inducer in Vitiligo}, journal = {Pharmacognosy Journal}, volume = {14}, year = {2022}, month = {December 2022}, pages = {847-857}, type = {Research Article }, chapter = {847}, abstract = {

Introduction: Vitiligo is a pigmentation disorder characterized by loss of skin color (depigmentation) due to melanocyte dysfunction and loss. Melanocytes produce melanin pigment through a melanogenesis process. Melanocyte survival and melanogenesis process are influenced by Microphthalmia Associated- Transcription Factor (MITF) and several proteins, including WNT, β-catenin, tyrosinase, Tyrosinase- Related Protein-1 (TRP1), and Tyrosinase-Related Protein-2 (TRP2). The current therapy for vitiligo is still unsatisfactory. Naringenin is one of Rhizophora mucronata compound, one type of mangrove plant often found in the eastern coastal area of Surabaya City. Objective: To investigate the naringenin{\textquoteright}s potency in melanogenesis and to predict the pharmacokinetics or toxicity of naringenin by in silico study. Methods: This is a computational study using a molecular docking method to observe the interaction of naringenin with WNT, β-catenin, MITF, tyrosinase, TRP-1, and TRP-2 proteins. Pharmacokinetic or toxicity prediction of naringenin using the pkCSM method. Psoralen was used as a control. Results: Naringenin binds to all these proteins in the same region as psoralen, indicating that naringenin can stimulate melanogenesis. Naringenin has lower binding energy than psoralen on all proteins (except β-catenin), indicating that naringenin{\textquoteright}s interaction with these proteins is stronger than psoralen. Pharmacokinetic and toxicity predictions show that naringenin has good absorption or permeation, is not mutagenic, is not hepatotoxic, and does not cause skin sensitization. Conclusion: This computational study concludes that naringenin has melanogenesis inducer potency and good pharmacokinetics.

}, keywords = {Mangrove, Naringenin, Rhizophora mucronata, Vitiligo, WNT}, doi = {10.5530/pj.2022.14.178}, author = {Dian Ardiana and Lestari Dewi and Renata Prameswari} } @article {1172, title = {Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways}, journal = {Pharmacognosy Journal}, volume = {12}, year = {2020}, month = {June 2020}, pages = {742-748}, type = {Original Article}, chapter = {742}, abstract = {

Background: Cadmium can induce pancreatic injury via oxidative stress, inflammation and apoptosis. Naringenin (NGN) and vanillin (VLN) exert antioxidant, anti-inflammatory, and antiapoptotic effects. Objective: The likely ameliorative effects of NGN, VLN and their combination were studied in rats exposed to cadmium-induced pancreatic injury. Materials and Methods: Rats received NGN (50 mg/kg/day, p.o.), VLN (100 mg/ kg/day, p.o.), or NGN + VLN for 7 days and one injection of CdCl2 (2 mg/kg, i.p.) on the 6th day. Results: Cadmium significantly lowered serum amylase and insulin levels. Cadmium also caused significant increments of malondialdehyde, tumor necrosis factor-α, interleukin-1β, nuclear factor-κB p65, Bax/Bcl-2 ratio and phosphorylated c-Jun N-terminal kinase (p-JNK) and p38 mitogen-activated protein kinases (MAPKs) and significant decrements of reduced glutathione and catalase in the pancreas of rats received CdCl2. Additionally, CdCl2 caused marked histopathological necrosis and significantly increased caspase-3 expression in pancreatic tissue. The cadmium-induced biochemical, histopathological and immunohistochemical changes were significantly ameliorated by NGN, VLN and NGN + VLN. However, NGN + VLN caused more significant ameliorative effects than did NGN and VLN alone. Conclusion: NGN, VLN and NGN + VLN afforded significant protection of pancreas in rats exposed to cadmium insult through modulation of JNK and p38 MAPK pathways and inhibition of oxidative stress, inflammation and apoptosis.

}, keywords = {CdCl2, JNK/MAPK, Naringenin, p38/MAPK, Pancreas, Vanillin}, doi = {10.5530/pj.2020.12.107}, author = {Amr A Fouad and Entesar F Amin and Amira F Ahmed} }