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Aim: To observe the effects of stearic acid against oxidative stress in primary cultured cortical neurons. Methods: Cortical neurons were exposed to glutamate, hydrogen peroxide (H 2 O 2 ), or NaN 3 insult in the presence or absence of stearic acid. Cell viability of cortical neurons was determined by MTT assay and LDH release. Endogenous antioxidant enzymes activity[superoxide dismutases (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT)] and lipid peroxidation in cultured cortical neurons were evaluated using commercial kits.5 µmol/L; a noncompetitive inhibitor of proliferator-activated receptor (PPAR)α], bisphenol A diglycidyl ether (BADGE; 100 µmol/L; an antagonist of PPARγ), and cycloheximide (CHX; 30 µmol/L, an inhibitor of protein synthesis) were tested for their effects on the neuroprotection afforded by stearic acid. Western blotting was used to determine the PPARγ protein level in cortical neurons. Results: Stearic acid dose-dependently protected cortical neurons against glutamate or H 2 O 2 injury and increased glutamate uptake in cultured neurons. This protection was concomitant to the inhibition of lipid peroxidation and to the promotion activity of Cu/Zn SOD and CAT in cultured cortical neurons. Its neuroprotective effects were completely blocked by BADGE and CHX. After incubation with H 2 O 2 for 24 h, the expression of the PPARγ protein decreased significantly (P<0.05), and the inhibitory effect of H 2 O 2 on the expression of PPARγ can be attenuated by stearic acid. Conclusion: Stearic acid can protect cortical neurons against oxidative stress by boosting the internal antioxidant enzymes. Its neuroprotective effect may be mainly mediated by the activation of PPARγ and new protein synthesis in cortical neurons.

Aim: To observe the effects of stearic acid, a long-chain saturated fatty acid consisting of 18 carbon atoms, on brain (cortical or hippocampal) slices insulted by oxygen-glucose deprivation (OGD), glutamate or sodium azide (NaN 3 ) in vitro. Methods: The activities of hippocampal slices were monitored by population spikes recorded in the CA1 region. In vitro injury models of brain slice were induced by 10 min of OGD, 1 mmol/L glutamate or 10 mmol/L NaN 3 . After 30 min of preincubation with stearic acid (3-30 µmol/L), brain slices (cortical or hippocampal) were subjected to OGD, glutamate or NaN 3 , and the tissue activities were evaluated by using the 2,3,5-triphenyltetrazolium chloride method. MK886 [5 mmol/L; a noncompetitive inhibitor of proliferator-activated receptor (PPAR-α)] or BADGE (bisphenol A diglycidyl ether; 100 µmol/L; an antagonist of PPAR-γ) were tested for their effects on the neuroprotection afforded by stearic acid. Results: Viability of brain slices was not changed significantly after direct incubation with stearic acid. OGD, glutamate and NaN 3 injury significantly decreased the viability of brain slices. Stearic acid (3-30 µmol/L) dose-dependently protected brain slices from OGD and glutamate injury but not from NaN 3 injury, and its neuroprotective effect was completely abolished by BADGE. Conclusion: Stearic acid can protect brain slices (cortical or hippocampal) against injury induced by OGD or glutamate. Its neuroprotective effect may be mainly mediated by the activation of PPAR-γ.

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The striped flea beetle (SFB) Phyllotreta striolata (Fabricius) (Coleoptera: Chrysomelidae) is a major pest of cruciferous vegetables in southern China. The population diversity and genetic structure of SFB are unknown. Here, we assembled a draft genome for the SFB and characterized the distribution of microsatellites. Then, we developed 12 novel microsatellite markers across the genome. We used a segment of the cox1 gene and newly developed microsatellite markers to genotype the genetic diversity of SFB across southern China. There were 44 mitochondrial haplotypes in the SFB populations, with haplotype 2 as the most widespread. The population genetic differentiation was very low, indicated by FST-values (&lt;0.05 except for Guangxi population with other populations based on cox1), high gene flow (4.10 and 44.88 of cox1 and microsatellite, respectively) and Principal Coordinate Analysis across all populations. Mantel test showed genetic distance in SFB was significantly associated with geographic distance based on microsatellites (R2 = 0.2373, P = 0.014) while result based on cox1 (R2 = 0.0365, P = 0.155) showed no significant difference. The phylogenetic analysis did not find any geographically related clades among all haplotypes. Analyses based on microsatellites showed a lack of population genetic structure among all populations. Our study provides a foundation for the future understanding of the ecology and evolution of SFB and its management.