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Mesenchymal stem cell transplantation can regulate neuroinflammation and treat Alzheimer's disease (AD), but its effect is attenuated by in vitro expansion. To solve this problem, we used tanshinone IIA (TIIA)-incubated mesenchymal stem cells (MSCs) to treat neuroinflammation caused by amyloid β-protein (Aβ). Here, we demonstrated that behavioral performance was rescued in rats receiving an intracerebroventricular injection of TIIA-incubated MSCs (TIIA-MSCs), and the TIIA-MSCs protected against neurotoxicity in the rat hippocampus by suppressing Aβ25-35-induced neuroinflammation. The levels of interleukin-1 (IL-1), IL-4, IL-6, IL-10 and tumor necrosis factor α (TNF-α) in Aβ25-35-induced rats were attenuated by TIIA-MSCs treatment, and IL-6 was the key difference between the TIIA-MSCs and MSCs groups. Furthermore, TIIA-MSCs reduced Aβ production-related mRNA (BACE1 and PS1) expression but had no significant effect on clearance (AMDM10). TIIA-MSCs also had the same effects on the protein levels. For the first time, we found that TIIA-MSCs have greater neuroprotective effects and prevent toxic protein production better than MSCs. These effects are related to Aβ modulation via downregulated BACE1 expression that promotes the survival of hippocampal neurons, as well as regulates neuroinflammatory-associated cytokines. These results provide support for the clinical application of MSCs, which will bring new hope for the treatment of AD.



Beta-caryophyllene (BCP) is a phytocannabinoid possessing selective agonistic activity to cannabinoid type-2 receptors (CB2R) and peroxisome proliferator-activated receptors-α (PPAR-α). However, few studies reported the contribution of PPAR-γ receptors in BCP effects. The aim of this study was to investigate the BCP effects on diet-induced dyslipidemia and vascular inflammation as well as the involvement of CB2R and PPAR-γ receptors. Wistar rats were fed a high-fat diet and administered 10% fructose for 12 weeks. Treatment with pioglitazone, BCP, BCP + CB2R antagonist, AM630, or BCP + PPAR-γ antagonist, BADGE was started from the 9th week and continued till the 12th week. BCP significantly ameliorated all diet-induced alterations in a CB2R-dependant manner as it improved glycemic parameters, dyslipidemia, and vascular oxidative stress and inflammation. It also downregulated proatherogenic adhesion molecule (VCAM-1) and restored vascular eNOS/iNOS expression balance. PPAR-γ was involved in BCP-evoked suppression of vascular inflammation, VCAM-1 and restoration of normal vascular eNOS/iNOS balance thus normal NO level. Furthermore, part of BCP hypolipidemic effects (lowering total cholesterol, LDL, VLDL) involved both CB2R and PPAR-γ receptors. BCP treatment was superior to pioglitazone in anti-inflammatory and anti-atherosclerotic measures. BCP may represent a more potent alternate to pioglitazone avoiding its side effects in the treatment of insulin resistance and vascular inflammation.



Drug-induced liver toxicity is the most frequent cause of acute liver failure worldwide. Hepatotoxicity caused by acetaminophen (ACT) overdose is mediated by its metabolic product promoting oxidative stress and activation of inflammatory mediators. Nuclear factor erythroid-related factor-2 (Nrf-2) induces the release of cytoprotective enzymes in response to electrophilic or oxidative stress and is considered a promising therapeutic target. Dimethyl fumarate (DMF) is a potent activator of (Nrf-2), its anti-inflammatory and antioxidant properties of DMF have been highlighted recently. We designed this study to explore the effect of DMF (100?mg/kg, orally) administered once and twice on hepatotoxicity induced by acetaminophen (ACT, 500?mg/kg, i.p.) in mice. DMF administration enhanced ACT-induced parameters in liver function, inhibited apoptosis and ameliorated the antioxidant machinery and inflammatory markers in a Nrf-2-dependent fashion. DMF elevated Nrf-2 and HO-1 levels and ameliorated liver injury as indicated by lowered levels of serum aminotransferases, ALP, GGT and bilirubin levels. Hepatic (Bcl-2) was elevated whereas hepatic caspase-3, NFκ-B, TNF-α and MPO were reduced. Hepatic levels of GSH, SOD, MDA and NO were altered promoting the antioxidant machinery. Histological examination of liver has further supported these results. These findings suggest that DMF can be employed in the treatment ACT-induced liver injury acting primarily through targeting Nrf-2/HO-1 pathway.

Acetylshikonin stimulates glucose uptake in L6 myotubes via a PLC-β3/PKCδ-dependent pathway

Posted by WD Huang, JC Zeng, ZC Liu, et al. on 2019-03-01 10:35:00



Acetylshikonin, a naphthoquinone derivative derived from Lithospermum erythrorhizon, has been shown to have various pharmacological activities; however, its effect on diabetes has rarely been reported. We investigated the hypoglycemic effect of acetylshikonin and found that it decreased blood glucose to a greater extent than insulin and improved glucose tolerance in mice. It also increased glucose uptake in L6 myotubes by inducing the expression and translocation of glucose transporter 4 via decomposition of phosphatidylinositol, increased generation of diacylglycerol, and activation of protein kinase C delta cascades; this is an insulin-, reactive oxygen species-, and AMP-activated protein kinase-independent pathway for glucose uptake. Our findings highlight the antidiabetic potential of acetylshikonin via a possible novel pathway for glucose uptake in L6 myotubes.



Inflammation and oxidative stress are the two processes crucial in atherogenesis. Platelet-activating factor acetylhydrolase (PAF-AH), a plasma lipoprotein-associated enzyme, degrades pro-inflammatory lipids generated within oxidatively modified lipoproteins. Extensive evidence shows that incretin-based drugs, a new class of anti-diabetic agents, can provide cardiovascular protection that cannot be attributed to their glucose-lowering effects. The present study was undertaken to determine whether the antiatherogenic effects of the GLP-1(glucagon-like peptide-1) receptor agonist (exenatide) and DPP-4(dipeptidyl peptidase-4) inhibitors (sitagliptin) may occur via the regulation of platelet-activating factor acetylhydrolase (PAF-AH) activity/mass and inhibition of low-density lipoprotein (LDL) oxidation in the fructose-fed rats.


Normal and fructose-fed rats (8 wk) were treated (4 wk) with sitagliptin (5 and 10 mg/kg p.o.) or with exenatide (5 and 10 μg/kg, s.c.). Plasma PAF-AH activity and phosphatidylcholine (PC) concentration were measured colorimetrically. Plasma PAF-AH concentration, oxidized LDL (oxLDL), hexanoyl-Lys adduct (HEL), lyso-PC, apolipoprotein A-I (apoA-I), apoB, platelet-activating factor (PAF), monocyte chemoattractant protein-1 (MCP-1) and endothelin-1 (ET-1) were measured by ELISA.


The four-week exenatide (5 μg/kg, sc.) treatment of fructose fed-rats significantly increased plasma PAF-AH activity (+33%, P<0.001) and decreased the level of circulating oxLDL (-42%, P<0.05) and MCP-1 (-23%, P<0.01). These changes were accompanied by the decrease in plasma PC/lyso-PC (-47%, P<0.001) and apoB/apoA-I ratio (-75%, P<0.001). The effect of exenatide on enzyme activity was associated with only a minor effect on metabolic parameters and was independent of weight reduction.


Exenatide but not sitagliptin inhibits oxidative modification of LDL probably due to favorable effect on plasma PAF-AH activity.

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