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Background: Skin pigmentation is modulated by various processes, with melanogenesis playing a key role. Melanin is synthesized by the catalysis of melanogenesis‐related enzymes, such as tyrosinase and tyrosine‐related proteins TRP‐1 and TRP‐2. Paeoniflorin is the main bioactive component of Paeonia suffruticosa Andr., Paeonia lactiflora., or Paeonia veitchii Lynch and has been used for centuries for its anti‐inflammatory, anti‐oxidant, and anti‐carcinogenic properties. Aims & methods: In this study, melanin biosynthesis in mouse melanoma (B16F10) cells was induced using α‐melanocyte‐stimulating hormone (α‐MSH), and then cells were co‐treated with paeoniflorin to evaluate its potential anti‐melanogenic effect. Results: α‐MSH stimulation increased melanin content, tyrosinase activity, and melanogenesis‐related markers in a dose‐dependent manner. However, treatment with paeoniflorin reversed α‐MSH‐induced upregulation of melanin content and tyrosinase activity. Furthermore, paeoniflorin inhibited cAMP response element‐binding protein activation and TRP‐1, TRP‐2, and microphthalmia‐associated transcription factor protein expression in α‐MSH‐stimulated B16F10 cells. Conclusion: Overall, these findings show the potential of paeoniflorin as a depigmenting agent for cosmetic products. [ABSTRACT FROM AUTHOR]

Lindane is a man-made organochlorine pesticide used for agricultural purposes. Since lindane-induced toxicity is mediated by free radical generation, this investigation was carried out to study the protective effects of gallic acid and quercetin against lindane-induced cardiotoxicity. Lindane (100 mg-[(kg body mass).sup.-1]) was administered orally to rats for 30 days. Histological analysis revealed pathological changes in the heart of lindane-treated rats. Biochemical analysis of the lindane-treated animals showed elevated activity for serum marker enzymes, lipid peroxidation (LPO), and membrane-bound [Ca.sup.2+] ATPase, with a concomitant decrease in the level of non-enzymic antioxidant (GSH), enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST), and membrane-bound ATPases like [Na.sup.+]/[K.sup.+] ATPase and [Mg.sup.2+] ATPase in heart tissue. The results suggest that gallic acid and quercetin offer protection against lindane-induced myocardial damage, possibly through maintaining levels of endogenous antioxidant enzymes and membrane bound ATPase activity, as well as inhibiting lipid peroxidation. Key words: antioxidants, ATPases, gallic acid, lindane, quercetin. Le lindane est un pesticide organochlore synthetique utilise a des fins agricoles. La toxicite induite par le lindane faisant intervenir la generation de radicaux libres, la presente etude a ete realisee afin d'etudier l'effet protecteur de l'acide gallique et de la quercetine contre la cardiotoxicite induite par le lindane. Le lindane (100 mg-(kg de poids corporel)-1) a ete administre oralement pendant 30 jours. L'analyse en histologie a revele des changements pathologiques dans le cceur des rats ayant recu du lindane. L'analyse biochimique du tissu cardiaque des animaux traites au lindane a revele une elevation de l'activite de marqueurs seriques enzymatiques, de la peroxydation des lipides (LPO) et de la [Ca.sup.2+] ATPase membranaire, de maniere concomitante a une diminution des niveaux d'antioxydants non enzymatiques (GSH), d'antioxydants enzymatiques comme la superoxyde dismutase, la catalase, la glutathion peroxydase (GPx) et la glutathion-S-transferase (GST), ainsi que les ATPases de la membrane comme la [Na.sup.+]/[K.sup.+] ATPase et la [Mg.sup.2+] ATPase. Les resultats suggerent que l'acide gallique et la quercetine offrent une protection contre le dommage myocardique induit par le lindane, possiblement en maintenant l'activite des enzymes anti-oxydantes endogenes et l'activite des ATPases liees a la membrane, et en inhibant la peroxydation des lipides. [Traduit par la Redaction] Mots-cles: antioxydants, ATPases, acide gallique, lindane, quercetine., Introduction The environmental toxins that cause the most problems are pesticides, solvents, and heavy metals. Lindane (7-hexacholorocyclohexane), an organochlorine pesticide used to eradicate insects in agriculture, to control malaria, and [...]

Aim: The current study was designed to investigate the effect of berbamine (BBM) on isoproterenol (ISO) induced changes in cardiac marker enzymes, myocardial oxidative stress, lipid profile and expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in male Wistar rats. Rats were pretreated with BBM (25 mg/kg) through intraperitoneal injection for 7 days followed by induction of myocardial infarction (MI) by subcutaneous injection of ISO (85 mg/kg) for last two days. Key findings: In the present study, the histopathological findings of the heart tissue showed that BBM treatment significantly minimized the damage induced by ISO. BBM pretreatment showed a significant decrease in heart weight, serum marker enzymes, lipid peroxidation and significant increase in cardiac endogenous enzymatic and non-enzymatic antioxidants compared to the ISO-treated group. In addition, we observed significantly upregulated eNOS expression and downregulated iNOS expression in BBM pretreated group. Thus, BBM protected the rat's heart from ISO-induced myocardial infarction by its antioxidant, and antilipidemic properties. Significance: The results of the present investigation suggested that BBM efficiently ameliorated the ISO-induced myocardial infarction in rats. [ABSTRACT FROM AUTHOR]

Combination of dietary components with chemotherapy drugs is an emerging new strategy for cancer therapy to increase antitumor responses. Neferine, major bisbenzylisoquinoline alkaloid isolated from the seed embryo of Nelumbo nucifera (Lotus). In the present study, we investigated the efficacy of the combinatorial regimen of neferine and cisplatin compared to cisplatin high dose in human lung adenocarcinoma (A549) cells. Co-treatment with neferine enhanced cisplatin-induced autophagy in A549 cells was accompanied by Acidic vesicular accumulation (AVO), enhanced generation of reactive oxygen species (ROS) and depletion of intracellular glutathione (GSH), down regulation of PI3K/AKT/mTOR pathway, conversion of LC3B-I to LC3B-II. This enhanced autophagy developed via a non-canonical mechanism that did not require Beclin-1, PI3KCIII. In conclusion, these results suggest that neferine enhances cisplatin-induced autophagic cancer cell death through downregulation of PI3K/Akt/mTOR signaling pro-survival pathway and ROS- mediated Beclin-1 and PI3K CIII independent autophagy in human lung adenocarcinoma (A549 cells). [ABSTRACT FROM AUTHOR]