ABSTRACT
Objective: To evaluate the protective effect of peanut sprout extract (PSE) against paraquat (PQ) induced SK-N-SH cells. Methods: Three groups of cells were used in the experiment, together with a fourth, control group. One group was treated with PQ, the second group was treated with PSE, and the third group was pre-treated with PSE. The control group was untreated. Cell viability and toxicity were detected by MTT assay, cellular reactive oxygen species (ROS) was detected by Muse Cell Analyzer, quantitative RT-PCR was applied to investigate the expression of SIRT1 and a-synuclein genes, and Ab42 was detected by western blot. Results: The 50% effective concentration of PQ was 0.75 mmol/L. PSE had no sig-nificant cytotoxicity at a concentration of 1.5 mg/mL. In the group of cells pre-treated with PSE, cell death was significantly inhibited. In the PQ treated group, PQ was increased in the intracellular ROS in the cells. Intracellular ROS was significantly decreased in the cells treated with PSE and also those pre-treated with PSE. PSE significantly downregulated the expression of SIRT1 and a-syn genes, and it was found that PQ significantly increased b-amyloid 42 levels whereas this action was inhibited by PSE. Conclusions: PSE has neuroprotective activities against oxidative stress in SK-N-SH cells induced by PQ, suggesting that PSE is a highly promising agent in the preven-tion of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
ABSTRACT
Objective To evaluate the protective effect of peanut sprout extract (PSE) against paraquat (PQ) induced SK-N-SH cells. Methods Three groups of cells were used in the experiment, together with a fourth, control group. One group was treated with PQ, the second group was treated with PSE, and the third group was pre-treated with PSE. The control group was untreated. Cell viability and toxicity were detected by MTT assay, cellular reactive oxygen species (ROS) was detected by Muse Cell Analyzer, quantitative RT-PCR was applied to investigate the expression of SIRT1 and α-synuclein genes, and Aβ42 was detected by western blot. Results The 50% effective concentration of PQ was 0.75 mmol/L. PSE had no significant cytotoxicity at a concentration of 1.5 mg/mL. In the group of cells pre-treated with PSE, cell death was significantly inhibited. In the PQ treated group, PQ was increased in the intracellular ROS in the cells. Intracellular ROS was significantly decreased in the cells treated with PSE and also those pre-treated with PSE. PSE significantly downregulated the expression of SIRT1 and α-syn genes, and it was found that PQ significantly increased β-amyloid 42 levels whereas this action was inhibited by PSE. Conclusions PSE has neuroprotective activities against oxidative stress in SK-N-SH cells induced by PQ, suggesting that PSE is a highly promising agent in the prevention of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
ABSTRACT
BACKGROUD/OBEJECTIVES: This study aims to find out the effects of peanut sprout extracts on weight controls and protein expressions of transcription factors related to adipocyte differentiation and adipocytokine in rats under high-fat diets. MATERIALS/METHODS: Four week-old Sparague-Dawley (SD) were assigned to 4 groups; normal-fat (NF) diets (7% fat diet), high-fat (HF) diets (20% fat diet), high fat diets with low peanut sprout extract (HF + PSEL) diet (20% fat and 0.025% peanut sprout extract), and high fat diets with high peanut sprout extract (HF + PSEH) diet (20% fat and 0.05% peanut sprout extract). Body weight changes, lipid profiles in adipose tissue, and the mRNA protein expressions, such as peroxisome proliferator-activated receptor gamma (PPARgamma), CCAAT element binding protein alpha (C/EBP alpha), leptin, and adiponectin, were determined. RESULTS: After 9 weeks of feeding, the HF + PSEH group had significantly less weight gains than the HF group (P < 0.05). However, the total dietary intakes or food efficiency ratios among groups were not significantly different. The weight of epididymal fat in HF + PSEH group, 3.61 +/- 0.5 g, or HF + PSEL group, 3.80 +/- 0.7 g, was significantly lower than the HF group, 4.39 +/- 0.4g, (P < 0.05). Total lipids and total cholesterol in adipose tissue were significantly decreased in HF + PSEH group compared to those in the HF group, respectively (P < 0.05). PSEH supplementation caused AST and ALT levels to decrease when it compared to HF group, but it was not statistically significant. The protein expression of PPARgamma in HF + PSEH group was significantly lower than the HF group (P < 0.05). Comparing with the HF group, the protein expression of adiponectin in HF + PSEH group was significantly increased (P < 0.05). The protein expressions of C/EBP alpha and leptin in HF + PSEH group were lower than the HF group, but it was not statistical significant. CONCLUSIONS: In conclusion, peanut sprout extract has anti-obesity effect by lowering the expressions of PPARgamma which regulates the expression of adiponectin.
Subject(s)
Animals , Rats , Adipocytes , Adiponectin , Adipose Tissue , Body Weight Changes , Carrier Proteins , Cholesterol , Diet , Diet, High-Fat , Leptin , Obesity , PPAR gamma , RNA, Messenger , Transcription Factors , Weight GainABSTRACT
3T3-L1 preadipocyte were differentiated to adipocytes, and then treated with 0, 10, 20, and 40 microg/mL of peanut sprout ethanol extract (PSEE). The main component of PSEE is resveratrol which contained 5.55 mg/mL of resveratrol. The MTT assay, Oil-Red O staining, glycerol-3-phosphate dehydrogenase (GPDH) activity, and the triglyceride concentration were determined in 3T3-L1 cells. MMP-2 and MMP-9 activities as well as mRNA expressions of C/EBP beta and C/EBP alpha were also investigated. As the concentration of PSEE in adipocytes increased, the cell proliferation was decreased in a dose-dependent manner from 4 days of incubation (P < 0.05). The GDPH activity (P < 0.05) and the triglyceride concentration (P < 0.05) were decreased as the PSEE treatment concentration increased. The mRNA expression of C/EBPbeta in 3T3-L1 cells was significantly low in groups of PSEE-treated, compared with control group (P < 0.05). The MMP-9 (P < 0.05) and MMP-2 (P < 0.05) activities were decreased in a dose-dependent manner as the PSEE concentration increased from 20 microg/mL. In conclusion, it was found that PSEE has an effect on restricting proliferation and differentiation of adipocytes.