Neuroprotective effects of macranthoin G from Eucommia ulmoides against hydrogen peroxide-induced apoptosis in PC12 cells via inhibiting NF-κB activation

Jiang

et al. 2016

IJMS

Self Cite

Chloranthalactone B (CTB), a lindenane-type sesquiterpenoid, was obtained from the Chinese medicinal herb Sarcandra glabra, which is frequently used as a remedy for inflammatory diseases. However, the anti-inflammatory mechanisms of CTB have not been fully elucidated. In this study, we investigated the molecular mechanisms underlying these effects in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. CTB strongly inhibited the production of nitric oxide and pro-inflammatory mediators such as prostaglandin E2, tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 in RAW264.7 cells stimulated with LPS. A reverse-transcription polymerase chain reaction assay and Western blot further confirmed that CTB inhibited the expression of inducible nitric oxide synthase, cyclooxygenase-2, TNF-α, and IL-1β at the transcriptional level, and decreased the luciferase activities of activator protein (AP)-1 reporter promoters. These data suggest that inhibition occurred at the transcriptional level. In addition, CTB blocked the activation of p38 mitogen-activated protein kinase (MAPK) but not c-Jun N-terminal kinase or extracellular signal-regulated kinase 1/2. Furthermore, CTB suppressed the phosphorylation of MKK3/6 by targeting the binding sites via formation of hydrogen bonds. Our findings clearly show that CTB inhibits the production of inflammatory mediators by inhibiting the AP-1 and p38 MAPK pathways. Therefore, CTB could potentially be used as an anti-inflammatory agent.

Section: Methodsmentioning

confidence: 99%

Anti-Inflammatory Effects of Chloranthalactone B in LPS-Stimulated RAW264.7 Cells

Jiang

et al. 2016

IJMS

Self Cite

“…The malondialdehyde (MDA) content of PC12 cells in each group was detected to assess the levels of membrane lipid peroxidation as previously described [12]. Briefly, 100 μl supernatant was collected and mixed with 1.5 ml acetic acid (20%), 1.5 ml thiobarbituric acid (0.8%), and 200 μl sodium dodecyl sulphate (SDS) (8%).…”

Section: Detection Of Lipid Peroxidationmentioning

confidence: 99%

Resveratrol protects PC12 cells against OGD/R-induced apoptosis via the mitochondrial-mediated signaling pathway

Liu

Zhu

Chen

et al. 2016

ABBS

In this study, we investigated the neuroprotective potential of resveratrol against oxygen glucose deprivation/reoxygenation (OGD/R)-induced apoptotic damages in well-differentiated PC12 cells and the underlying mechanisms. Cells were incubated under normal condition or OGD/R in the presence or absence of 10 μM resveratrol. Cell viability was determined with methyl-thiazolyl-tetrazolium (MTT) assay. Apoptotic ratio was determined with Hoechst 33342 staining and Annexin V-FITC/PI double staining. Oxidative stress was evaluated by measuring the intracellular reactive oxygen species (ROS), the mitochondrial superoxide, the malondialdehyde (MDA) content, and the activities of superoxide dismutase (SOD) and catalase (CAT). The intracellular calcium ([Ca 2+ ]i) was estimated by Fluo-3/ AM. The mitochondrial membrane potential (MMP) was evaluated by 5,5′,6,6′-tetrachloro-1,1,3,3′-tetraethyl-benzimidazolyl-carbocyanine iodide (JC-1) and rhodamine 123 (Rh123). The opening of mitochondrial permeability transition pore (MPTP) was determined by the Calcein/Co 2+ -quenching technique. The protein levels of cytochrome c, Bcl-2, Bax, cleaved caspase-9, and cleaved caspase-3 were detected by western blot analysis. The results showed that 10 μM resveratrol attenuated OGD/R-induced cell viability loss and cell apoptosis, which was associated with the decreases in the MDA content and the increases in the SOD and CAT activities. Furthermore, the accumulation of intracellular ROS and mitochondrial superoxide, disturbance of [Ca 2+ ]i homeostasis, reduction of MMP, opening of MPTP, and release of mitochondrial cytochrome c observed in OGD/R-injured cells, which indicated a switch on the mitochondrial-mediated apoptotic pathway, were all reversed by resveratrol. These results suggest that resveratrol administration may play a neuroprotective role via modulating the mitochondrial-mediated signaling pathway in OGD/R-induced PC12 cell injury.

“…HepG2 cells (5 9 10 4 /well) were plated in a 96-well plate for 16 h. Then, the medium was aspirated and replaced with serum-free medium of different samples for 6 h. After removing the supernatant of each well, a total of 10 lL of MTT solution was added to each well at the time of incubation for 4 h. The formazan crystals were solubilized with 100 lL of MTT stop solution and measured using an Infinite M200 Pro spectrophotometer (Hu et al 2014). Cytoprotective activity of test samples on CCl 4 -induced cell injury was investigated.…”

Section: Hepatoprotective Activity Assaymentioning

confidence: 99%

Hepatoprotective effect of phenylethanoid glycosides from Incarvillea compacta against CCl4-induced cytotoxicity in HepG2 cells

J Korean Soc Appl Biol Chem

Zhang

et al. 2015

Self Cite

The extraction and solvent partition of roots of Incarvillea compacta, a traditional Tibetan folk medicine, and repeated column chromatography and preparative high-performance liquid chromatography for n-butanol fraction yielded four phenylethanoid glycosides, crenatoside (1), 3 000 -O-methylcrenatoside (2), leucoseceptoside A (3), and martynoside (4). The chemical structures were identified on the basis of spectroscopic data analyses including NMR and MS. All compounds were isolated for the first time from the plant. Compound 1 exerted better 1,1-diphenyl-2-picrylhydrazyl free radical scavenging activity. In addition, compounds 1-4 were evaluated for their hepatoprotective activity on carbon tetrachloride (CCl 4 )-induced liver injury in HepG2 cells. Pretreatment of HepG2 cells with compound 1-4 significantly increased the viability on CCl 4 -induced cell death. Furthermore, compounds 1-4 also alleviated CCl 4 -induced hepatotoxicity by enhancement of the antioxidant enzyme activities of superoxide dismutase and reduction of the malondialdehyde content, intracellular ROS as well as NF-jB transactivation. Our results suggest that phenylethanoid glycosides ameliorate CCl 4 -induced cell injury, and this protection was likely due to antioxidative activity and down-regulation of NF-jB.