[Molecular mechanism of apoptosis of breast cancer SKBR-3 cells induced by cryptanshinone via G protein coupled estrogen receptor( GPER) mediated pathway].

The study aimed to illuminate the role of G protein coupled estrogen receptor( GPER) and its mediated PI3 K/AKT signaling pathway in cryptotanshinone( CPT) induced apoptosis of breast cancer SKBR-3 cells,which is GPER positive and ER negative.The apoptosis rate of SKBR-3 cells was tested by Annexin V-FITC/PI staining and apoptosis effector caspase-3 was determined by Western blot. The key proteins in PI3 K/AKT signaling pathway mediated by GPER were detected by Western blot and immunofluorescence technique. Meanwhile,the agonist G1 and antagonist G15 of GPER and antagonist LY294002 of PI3 K were employed in the test to further clarify the effect of GPER and PI3 K/AKT pathway. The results indicated that the apoptosis rate was increased from 4. 7% to46. 1% and 69. 0% after treatment with 0,5,10 µmol·L~(-1) CPT for 48 h( P<0. 01). The expression of PI3 K,AKT and p-AKT were inhibited( P<0. 05 or P<0. 01),while caspase-3 level increased obviously after treatment with CPT( P<0. 01). Importantly,inhibitory effect of PI3 K/AKT signaling pathway by CPT was further enhanced by G1 and attenuated by G15. LY294002 also induced a further inhibition of expression of AKT and p-AKT. The mean fluorescence intensity of AKT and p-AKT could be decreased by CPT. Furthermore,CPT could downregulate GPER expression in SKBR-3 cells( P<0. 01),which could be inhibited by G1 and enhanced by G15.In conclusion,CPT could induce the apoptosis of ER negative and GPER positive breast cancer SKBR-3 cells and the molecular mechanism is related to its regulatory effect of GPER and its mediated PI3 K/AKT signaling pathway.

Microcapsules biologically prepared using Perilla frutescens (L.) Britt. essential oil and their use for extension of fruit shelf life.

BACKGROUND: Perilla essential oil (EO) possesses high antioxidant, antimicrobial and insecticidal activities, and has proven to be more reliable than chemically synthesized food preservatives. Nevertheless, EOs have disadvantages of facile photo-degradation and oxidation, which limit their use in agriculture and food industries. Microencapsulation technology that generates a polymeric coating surrounding EOs could overcome these disadvantages. RESULTS: The EO concentration had a significant effect on encapsulation efficiency (EE) and loading capacity (LC). The best encapsulation conditions were obtained with 2% v/v EO, for which EE and LC were 57% and 36%, respectively. EO-loaded microspheres exhibited a crimped surface with phanic lumps by scanning electron microscopy. Thermal stability experiments revealed droplets that began to decompose sharply at 108 °C, with a 61% weight, loss, which was much lower than EOs of 98%. EO-loaded microcapsules demonstrated good antibacterial activity. Strawberry preservation studies showed that EO-loaded microcapsules could significantly inhibit strawberry decay, maintain the quality of strawberries and prolong shelf life. CONCLUSION: Perilla EO-loaded microcapsules were successfully prepared by ionic gelation and were effective at inhibiting several bacterial strains. EO-alginate microcapsules could effectively delay the volatilization of EO. Perilla EO-loaded microcapsules therefore have potential for use as an antimicrobial and preservative agent in the food industry. © 2017 Society of Chemical Industry.

[Effects of beta-amyloid and apolipoprotein E4 on hippocampal choline acetyl transferase in rats].

OBJECTIVE: To investigate the effects of beta-amyloid (Aß) and apolipoprotein E4(apoE4) on choline acetyl transferase (ChAT) in hippocampus and to explore possible the synergistic effect of both Aß and apoE4. METHODS: Male Wistar rats were divided into four groups: control group, Aß group, apoE4 group and Aß + apoE4 group. Rats in different group received injection of normal saline, Aß1-40, apoE4 and Aß1-40 + apoE4, respectively, into bilateral hippocampus CA1 regions under the control of a brain stereotaxic apparatus. The learning-memory ability with the escape latency and the times of passing platform and the expression of ChAT in hippocampus CA1 regions were documented. RESULTS: The escape latency at fifth day and the times of passing platform and ChAT mRNA PU values were obtained for the control group (10.75 s ± 2.44 s, 4.13 ± 0.64, and 28.90 ± 4.43), apoE4 group (23.88 s ± 4.32 s, 2.38 ± 0.52, and 20.85 ± 3.98), Aß group (43.50 s ± 9.78 s, 1.38 ± 0.52, and 16.96 ± 2.53), and Aß + apoE4 group (70.63 s ± 10.04 s, 0.75 ± 0.71, and 13.01 ± 2.21). Through 5 days of training all animals acquired learning-memory ability with the gradually shortened escape latency, although injection of Aß1-40 and apoE4 all induced learning-memory damage, due to a significantly prolonged the escape latency at fifth day (P < 0.01) and markedly decreased the times of passing platform (P < 0.01) in both Aß and apoE4 group than in control group. An interaction between Aß and apoE4 also was observed, with further prolonged escape latency(P < 0.01). ChAT mRNA PU values were significantly lower in the Aß group and apoE4 group than in the control group (P < 0.01). Aß and apoE4 demonstrated interaction in lowering ChAT mRNA level(P < 0.05). CONCLUSIONS: Both Aß and apoE4 induce an injury to hippocampal cholinergic system and its learning-memory ability, in which Aß and apoE4 have a synergistic effect in the initiation of such injury.