Pseudoginsenoside-F11 alleviates oligomeric ß-amyloid-induced endosome-lysosome defects in microglia.

Amyloid accumulation in the brain is the major pathological hallmark of Alzheimer disease (AD). Amyloid beta (Aß) is cleared by the endosomal-autophagy-lysosomal system, which is impaired in AD pathogenesis by an unknown mechanism. Pseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside, has been demonstrated to decrease the level of Aß in APP/PS1 mouse brain and to protect neurons by inhibiting the activation of microglia in vitro. The present study showed that PF11 was capable of increasing the uptake and degradation of oligomeric Aß in cultured microglia. Oligomeric Aß (oAß) interrupted the autophagy-lysosomal degradative system by regulating the nuclear translocation of transcription factor EB (TFEB), a master factor in lysosomal biogenesis. Conversion of Rab5 to Rab7, which is important for the mechanism of cargo progression from early to late endosomes, was also interrupted by high-concentration oAß. Notably, in the PF11-treated microglial cells, a dramatic increase of the lysosome-associated proteins and enzyme expression were observed, along with the intracellular pH steady state, indicating the improvement of lysosomal function. In addition, PF11 induced TFEB nuclear translocation in microglia treated with high-concentration oAß. Furthermore, PF11 was able to restore Rab conversion, suggesting an effective role of PF11 in the maturation of endosomes. These data provide evidence that PF11 can reverse the dysfunction of the endosomal-lysosomal system induced by high-concentration oAß in microglia, and this might be the main mechanism by which PF11 facilitates oAß clearance. Accordingly, we propose that PF11 should be considered as a potential agent for treating AD.

Treatment of aging oily wastewater by demulsification/flocculation.

The aging oily wastewater (AOW) from Tarim oilfield in China was treated by demulsification/flocculation. A novel sewage treatment agent (YL-7) was developed using a cationic surfactant (LY) and flocculants (polydimethyl diallyl ammonium chloride (PDMDAAC)/polyaluminum chloride (PAC)). At an YL-7 dosage of 320 mg L(-1) at 323 K for 90 min, the oil content of AOW was reduced from 728.8 mg L(-1) to 23.7 mg L(-1), and oil removal efficiency reached 96.7%. Microorganism flocs (extracted from AOW) with high negative zeta potential enhanced the stability of oil/water emulsion. LY and PDMDAAC neutralized the negative charge on the oil droplet surface. PDMDAAC and PAC mainly bridged and swept flocs during the flocculation process. YL-7 was found to be a suitable sewage treatment agent in removing oil from AOW.

Lesions of nucleus accumbens affect morphine-induced release of ascorbic acid and GABA but not of glutamate in rats.

Our previous studies have shown that local perfusion of morphine causes an increase of extracellular ascorbic acid (AA) levels in nucleus accumbens (NAc) of freely moving rats. Lines of evidence showed that glutamatergic and GABAergic were associated with morphine-induced effects on the neurotransmission of the brain, especially on the release of AA. In the present study, the effects of morphine on the release of extracellular AA, γ-aminobutyric acid (GABA) and glutamate (Glu) in the NAc following bilateral NAc lesions induced by kainic acid (KA) were studied by using the microdialysis technique, coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD) and fluorescent detection (HPLC-FD). The results showed that local perfusion of morphine (100 µM, 1 mM) in NAc dose-dependently increased AA and GABA release, while attenuated Glu release in the NAc. Naloxone (0.4 mM) pretreated by local perfusion to the NAc, significantly blocked the effects of morphine. After NAc lesion by KA (1 µg), morphine-induced increase in AA and GABA were markedly eliminated, while decrease in Glu was not affected. The loss effect of morphine on AA and GABA release after KA lesion could be recovered by GABA agonist, musimol. These results indicate that morphine-induced AA release may be mediated at least by µ-opioid receptor. Moreover, this effect of morphine possibly depend less on the glutamatergic afferents, but more on the GABAergic circuits within this nucleus. Finally, AA release induced by local perfusion of morphine may be GABA-receptor mediated and synaptically localized in the NAc.