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Qingchang Suppository (QCS) is a Traditional Chinese Medicine formula (TCM) for Ulcerative Colitis (UC), which has been used for the treatment of UC for more than 30 years with therapeutic effect. This formula is optimized from a classic formula called "Qingdai San". Although some experiments have shown QCS effective for UC, its mechanism on UC is still unclear and needs to be clarified.

To investigate the usage of QCS in our hospital, clarify the main compounds in QCS and their anti-inflammation effect both in vivo and in vitro.

Prescription analysis was performed in the clinical department and pharmacology network prediction was predicted for relative signal pathways. 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced colitis rats and Lipopolysaccharide (LPS)-induced Caco-2cell as an inflammatory model were used to evaluate the effect of QCS.

QCS and its herbs were associated with inflammatory and immunological diseases. QCS and its ingredients showed little toxicity on Caco-2cell and could down-regulate the level of Interleukin-6 (IL-6) and expression of signal transducer and activator of transcription 3 (P-STAT3 Tyr705) in LPS-induced Caco-2cell. In an animal experiment, QCS and its ingredients (indigo and gallic acid) could alleviate the symptoms of TNBS-induced colitis of rats, significantly decrease pro-inflammatory factors and anti-inflammatory factors as well as inhibit the expressions of P-STAT3 and Tyr705.

QCS and its components could improve UC by anti-inflammation. JAK2/STAT3 pathway might be the possible signaling pathway.

QCS and its components could improve UC by anti-inflammation. JAK2/STAT3 pathway might be the possible signaling pathway.

Kyung-Ok-Ko (KOK), a traditional medicinal formula composed of Rehmannia glutinosa (Gaertn.) DC, Poria cocos (Schw.) Wolf, Korean Red Panax ginseng C.A.Mey, and honey, has been used to treat amnesia and dementia. KOK has also been shown to ameliorate transient cerebral global ischemia-induced brain damage, but the antidepressant-like effect of KOK has not been examined.

This study examined the antidepressant-like effect of KOK in an immobilization-induced stress mouse and its mechanisms of action.

The animals in the stress group were immobilized for two hours a day for two weeks. KOK at a dose of 1g/kg/day was administered orally to the stressed mice for two weeks in advance of their immobilization. A forced swimming test was performed to analyze their depressive behaviors. To examine the anti-inflammatory or antioxidative effects of KOK, the murine macrophage cell line, RAW 264.7cells and human neuroblastoma cell, SH-SY5Y cells, were treated with lipopolysaccharide (LPS) and hydrogen peroxide, respectively.

The KOK extract showed no significant toxicity when the cells were treated with a KOK extract at 5, 10, 25, 50, and 100μg/mL. The KOK ethanol extract reduced LPS-induced TNF-α production, inducible nitric oxide (iNOS) mRNA level, and the levels of MAPK and p38 phosphorylation in RAW 264.7cells. KOK also suppressed H

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-induced cell death and the production of reactive oxygen species (ROS) in SH-SY5Y cells. In the forced swimming test, KOK induced a decrease in immobility and an increase in climbing activity. Finally, the administration of KOK reversed the up-regulation of IkB-α phosphorylation in the stressed mouse cortex.

KOK might be useful for the treatment of depression caused by environmental and lifestyle-related stress.

KOK might be useful for the treatment of depression caused by environmental and lifestyle-related stress.

Acorn obtained from the Quercus liaotungensis Koidz tree is consumed as a Chinese folk medicine for the treatment of diarrhea, abdominal pain, and inflammation, also having strong antioxidant activity and have been utilized for the treatment of diabetes in China. However, its mechanism of action on complications of diabetes and oxidative stress is unclear.

The purpose of this research was to assess the effects of acorn (Quercus liaotungensis Koidz) ethanol extract (AE) on pancreatic β-cell dysfunction through a streptozotocin (STZ)-damaged mouse normal pancreatic β-cell (MIN6 cell) model in vitro, and by using a high-fat and high-sugar diet with STZ-induced diabetic rat model in vivo to explore the possible mechanism of action against diabetes.

MIN6 cells were pretreated with AE (20, 40, 80μM) for 2h and then treated with 3mM STZ for 24h. Cell viability was measured by MTT assay. The amount of intracellular reactive oxygen species was measured by 2,7-dichlorodi-hydrofluorescein diacetate. The activitiesE-administered group reduced pancreatic injury by significantly restoring the insulin content in β-islets. It was observed that the anti-diabetic effects of AE were associated with the suppressed the p38 MAPK pathway and actived the Nrf2 pathway.

The ameliorative impact of AE on diabetes may be attributed to protection of the function of pancreatic β islets and by improving serum insulin levels, hence reducing the blood glucose, which involved in the p38 MAPK and Nrf2 pathways.

The ameliorative impact of AE on diabetes may be attributed to protection of the function of pancreatic β islets and by improving serum insulin levels, hence reducing the blood glucose, which involved in the p38 MAPK and Nrf2 pathways.Microglia are brain-resident immune cells and regulate mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by a supernumerary chromosome 21, containing also genes related to the immune system. In the hippocampus of the Dp(16) mouse model of DS and DS individuals, we found activated microglia, as assessed by their morphology; activation markers; and, for DS mice, electrophysiological profile. learn more Accordingly, we found increased pro-inflammatory cytokine levels and altered interferon signaling in Dp(16) hippocampi. DS mice also showed decreased spine density and activity of hippocampal neurons and hippocampus-dependent cognitive behavioral deficits. Depletion of defective microglia or treatment with a commonly used anti-inflammatory drug rescued the neuronal spine and activity impairments and cognitive deficits in juvenile Dp(16) mice. Our results suggest an involvement of microglia in Dp(16)-mouse cognitive deficits and identify a new potential therapeutic approach for cognitive disabilities in DS individuals.