Ginsenoside Re, one of the main constituents of Panax ginseng, possesses novel antioxidant and anti-inflammatory properties. However, the pharmacological mechanism of ginsenoside Re in dopaminergic degeneration remains elusive. We suggested that protein kinase C (PKC) δ mediates methamphetamine (MA)-induced dopaminergic toxicity. Treatment with ginsenoside Re significantly attenuated methamphetamine-induced dopaminergic degeneration in vivo by inhibiting impaired enzymatic antioxidant systems, mitochondrial oxidative stress, mitochondrial translocation of protein kinase Cδ, mitochondrial dysfunction, pro-inflammatory microglial activation, and apoptosis. These protective effects were comparable to those observed with genetic inhibition of PKCδ in PKCδ knockout (-/-) mice and with PKCδ antisense oligonucleotides, and ginsenoside Re did not provide any additional protective effects in the presence of PKCδ inhibition. Our results suggest that PKCδ is a critical target for ginsenoside Re-mediated protective activity in response to dopaminergic degeneration induced by MA.

mice. Together, our findings suggest that the interaction between the dopaminergic system and leptin signaling in hypothalamus is important in control of energy homeostasis.Dopamine is the main catecholamine in the brain. It serves important regulatory roles in many neural functions, including the control of locomotion, neuroendocrine hormone release, cognition, emotive behavior, reward, and memory (1). Dopamine is also a critical neurotransmitter in the control of feeding behavior. It is generally accepted that the dopaminergic pathway is primarily involved in the regulation of reward-related behaviors, including feeding behaviors. Dopamine regulates these behaviors through the mesolimbic dopaminergic pathways, which project from the ventral tegmental area (VTA) 4 to the limbic region, including the nucleus accumbens. Dopamine signaling in these reward-related circuits seems to control for different reward values, including food rewards (2, 3).The cellular and molecular mechanism by which dopamine controls food intake through these dopaminergic mesolimbic pathways remains largely unknown. Recent findings propose that hormones regulating energy homeostasis, such as leptin and insulin, can modulate the midbrain dopaminergic system to regulate feeding behavior (4, 5). However, it is not known if the action of these hormones in VTA regions of the midbrain would be physiologically relevant, because there are very few functional receptors of leptin or insulin in this region (3-5). Dopamine is presumed to regulate feeding via hypothalamic circuits in the brain (6 -10). Dopaminergic neurons project to the arcuate nucleus and to the median eminence of the hypothalamus. These projections may influence the function of hypothalamic neurons involved in ingestive behaviors. Pharmacological studies using D 1 -and D 2 -like receptor agonists and antagonists demonstrated that modulation of dopamine receptor activity in the hypothalamus could regulate food intake (11-16). However, the mechanism by which dopaminergic neurotransmission in the hypothalamus regulates food intake has yet to be defined. Different reports on the role of dopamine on food intake have yielded contradictory results. Contradictions may be due to the differential actions of dopamine on different hypothalamic areas or the involvement of different receptor subtypes.Binding of dopamine to the dopamine D 2 receptor is crucial for the regulation of diverse physiological functions, such as the control of locomotor activity, reward-related behavior, and the *

No abstract

Camellia japonica oil (CJ oil) has been used traditionally in EastAsia to nourish and soothe the skin as well as help restore the elasticity of skin. CJ oil has also been used on all types of bleeding instances. However, little is known about its anti-inflammatory effects. Therefore, the anti-inflammatory effects of CJ oil and its mechanisms of action were investigated. CJ oil inhibited LPS-induced production of NO, PGE2, and TNF-α in RAW264.7 cells. In addition, expression of COX-2 and iNOS genes was reduced. To evaluate the mechanism of the anti-inflammatory activity of CJ oil, LPS-induced activation of AP-1 and NF-κB promoters was found to be significantly reduced by CJ oil. LPS-induced phosphorylation of IκBα, ERK, p38, and JNK was also attenuated. Our results indicate that CJ oil exerts anti-inflammatory effects by downregulating the expression of iNOS and COX-2 genes through inhibition of NF-κB and AP-1 signaling. [BMB reports 2012; 45(3): 177-182]

Therapeutic, IV.