Gintonin-Enriched Fraction Suppresses Heat Stress-Induced Inflammation Through LPA Receptor.

Heat stress can be caused by various environmental factors. When exposed to heat stress, oxidative stress and inflammatory reaction occur due to an increase of reactive oxygen species (ROS) in the body. In particular, inflammatory responses induced by heat stress are common in muscle cells, which are the most exposed to heat stress and directly affected. Gintonin-Enriched Fraction (GEF) is a non-saponin component of ginseng, a glycolipoprotein. It is known that it has excellent neuroprotective effects, therefore, we aimed to confirm the protective effect against heat stress by using GEF. C2C12 cells were exposed to high temperature stress for 1, 12 and 15 h, and the expression of signals was analyzed over time. Changes in the expression of the factors that were observed under heat stress were confirmed at the protein level. Exposure to heat stress increases phosphorylation of p38 and extracellular signal-regulated kinase (ERK) and increases expression of inflammatory factors such as NLRP3 inflammasome through lysophosphatidic acid (LPA) receptor. Activated inflammatory signals also increase the secretion of inflammatory cytokines such as interleukin 6 (IL-6) and interleukin 18 (IL-18). Also, expression of glutathione reductase (GR) and catalase related to oxidative stress is increased. However, it was confirmed that the changes due to the heat stress were suppressed by the GEF treatment. Therefore, we suggest that GEF helps to protect heat stress in muscle cell and prevent tissue damage by oxidative stress and inflammation.

Cardamonin suppresses lipogenesis by activating protein kinase A-mediated browning of 3T3-L1 cells.

BACKGROUND: Obesity develops when dietary energy intake exceeds energy expenditure, and can be associated with metabolic syndrome. Recent studies have shown that dietary phytochemicals can promote energy expenditure by inducing the browning of white adipose tissue (WAT). PURPOSE: This study investigated whether cardamonin induces the browning of 3T3-L1 adipocytes through the activation of protein kinase A (PKA). METHODS: Anti-obesity potential of cardamonin was evaluated in 3T3-L1 adipocytes. Adipocyte-specific genes were observed using western blot, qPCR analysis and immunocytochemistry. RESULTS: Cardamonin treatment inhibited lipid droplet accumulation and reduced the expression of the adipogenic proteins C/EBPα and FABP4, and the lipogenic proteins LPAATθ, lipin 1, DGAT1, SREBP1, and FAS. Cardamonin also induced the expression of the browning marker genes PRDM16, PGC1α, and UCP1 at the mRNA and protein levels, and induced mRNA expression of CD137, a key marker of beige adipocytes. It also increased the expression of the ß-oxidation genes CPT1 and PPARα at the mRNA and protein levels. In addition, cardamonin increased PKA phosphorylation and the mRNA and protein expression of the downstream lipolytic enzymes adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL). CONCLUSION: Our findings demonstrate novel effects of cardamonin to stimulate adipocyte browning, suppress lipogenesis, and promote lipolysis, implying it may have potential as an anti-obesity agent.

Korean ginseng extract ameliorates abnormal immune response through the regulation of inflammatory constituents in Sprague Dawley rat subjected to environmental heat stress.

BACKGROUND: Increases in the average global temperature cause heat stress-induced disorders by disrupting homeostasis. Excessive heat stress triggers an imbalance in the immune system; thus protection against heat stress is important to maintain immune homeostasis. Korean ginseng (Panax ginseng Meyer) has been used as a herbal medicine and displays beneficial biological properties. METHODS: We investigated the protective effects of Korean ginseng extracts (KGEs) against heat stress in a rat model. Following acclimatization for 1 week, rats were housed at room temperature for 2 weeks and then exposed to heat stress (40°C/2 h/day) for 4 weeks. Rats were treated with three KGEs from the beginning of the second week to the end of the experiment. RESULTS: Heat stress dramatically increased secretion of inflammatory factors, and this was significantly reduced in the KGE-treated groups. Levels of inflammatory factors such as heat shock protein 70, interleukin 6, inducible nitric oxide synthase, and tumor necrosis factor-alpha were increased in the spleen and muscle upon heat stress. KGEs inhibited these increases by down-regulating heat shock protein 70 and the associated nuclear factor-κB and mitogen-activated protein kinase signaling pathways. Consequently, KGEs suppressed activation of T-cells and B-cells. CONCLUSION: KGEs suppress the immune response upon heat stress and decrease the production of inflammatory cytokines in muscle and spleen. We suggest that KGEs protect against heat stress by inhibiting inflammation and maintaining immune homeostasis.

Spirulina maxima Extract Ameliorates Learning and Memory Impairments via Inhibiting GSK-3ß Phosphorylation Induced by Intracerebroventricular Injection of Amyloid-ß 1-42 in Mice.

Spirulina maxima, a microalga containing high levels of protein and many polyphenols, including chlorophyll a and C-phycocyanin, has antioxidant and anti-inflammatory therapeutic effects. However, the mechanisms where by Spirulina maxima ameliorates cognitive disorders induced by amyloid-ß 1-42 (Aß1-42) are not fully understood. In this study, we investigated whether a 70% ethanol extract of Spirulina maxima (SM70EE) ameliorated cognitive impairments induced by an intracerebroventricular injection of Aß1-42 in mice. SM70EE increased the step-through latency time in the passive avoidance test and decreased the escape latency time in the Morris water maze test in Aß1-42-injected mice. SM70EE reduced hippocampal Aß1-42 levels and inhibited amyloid precursor protein processing-associated factors in Aß1-42-injected mice. Additionally, acetylcholinesterase activity was suppressed by SM70EE in Aß1-42-injected mice. Hippocampal glutathione levels were examined to determine the effects of SM70EE on oxidative stress in Aß1-42-injected mice. SM70EE increased the levels of glutathione and its associated factors that were reduced in Aß1-42-injected mice. SM70EE also promoted activation of the brain-derived neurotrophic factor/phosphatidylinositol-3 kinase/serine/threonine protein kinase signaling pathway and inhibited glycogen synthase kinase-3ß phosphorylation. These findings suggested that SM70EE ameliorated Aß1-42-induced cognitive impairments by inhibiting the increased phosphorylation of glycogen synthase kinase-3ß caused by intracerebroventricular injection of Aß1-42 in mice.