Silver dendrite metasurface SERS substrates prepared by photoreduction method for perfluorooctanoic acid detection.

Perfluorooctanoic acid (PFOA), a novel organic pollutant, has been shown to be toxic, persistent, bioaccumulative, long-range transportable, and globally prevalent. This article is based on surface enhanced Raman scattering (SERS) spectroscopy analysis technology. The monolayer of SiO2 was prepared by chemical reduction etching self-assembly method and silver dendrites were grown on it, thus forming the SERS substrate with silver dendrite Metasurface structure with Raman detection enhancement factor up to 2.32 × 105. The prepared silver dendrite Metasurface SERS substrate was applied to the qualitative and quantitative detection of PFOA, with a quantitative detection limit of 15.89 ppb. The results of this paper provide a new, simple, and quick method for the detection of PFOA in the environment.

Anisotropic carrier dynamics and laser-fabricated luminescent patterns on oriented single-crystal perovskite wafers.

Perovskite materials and their applications in optoelectronics have attracted intensive attentions in recent years. However, in-depth understanding about their anisotropic behavior in ultrafast carrier dynamics is still lacking. Here we explore the ultrafast dynamical evolution of photo-excited carriers and photoluminescence based on differently-oriented MAPbBr3 wafers. The distinct in-plane polarization of carrier relaxation dynamics of the (100), (110) and (111) wafers and their out-of-plane anisotropy in a picosecond time scale were found by femtosecond time- and polarization-resolved transient transmission measurements, indicating the relaxation process dominated by optical/acoustic phonon interaction is related to photoinduced transient structure rearrangements. Femtosecond laser two-photon fabricated patterns exhibit three orders of magnitude enhancement of emission due to the formation of tentacle-like microstructures. Such a ultrafast dynamic study carried on differently-oriented crystal wafers is believed to provide a deep insight about the photophysical process of perovskites and to be helpful for developing polarization-sensitive and ultrafast-response optoelectronic devices.

Electron Density Changes and Ultrafast Carrier Dynamics of the Antiferromagnetic Semiconductor MnPS3 through Magnetic Phase Transition.

Studying ultrafast dynamics provides us with a way to modify materials from the timescale of particle interaction, and the related research on antiferromagnetic semiconductors is still inadequate. Based on the electron density reconstruction, we achieve the visualization of magnetic interactions of bulk antiferromagnetic MnPS3 in the ground state, reveal the role of two atomic site occupations of S atoms in different magnetic phase transitions, and provide the theoretical and experimental support for modifying magnetic properties by selectively replacing the S atom. The ultrafast carrier dynamics can provide information from the excited state to the ground state. Based on time-resolved transmittance measurements, ultrafast carrier dynamics of MnPS3 are reported. The phonon-assisted gap transition driven by the electronic structure is characterized. The coupling relationship among electrons, spin, and phonons is established. Furthermore, the spin orientations within different phases are confirmed.

Study on Spectral Selective Manipulation Characteristics of Surface Multilevel Micro-Nano Structures by FDTD Simulation.

The optical filter based on the micro-nano structure on the material surface is an important optical device, which is widely used in many fields. The filter is fabricated on the substrate with different shapes and sizes of micro-nano array structure, and the wavelength selectivity is realized by adjusting the processing parameters. In this paper, the finite-difference time-domain (FDTD) method is used to simulate the spectral properties of periodic array structures on the Au surface, and the spectral response characteristics of different surface structural parameters to the incident light are obtained. The simulation results show that the periodic pore array has a directional modulation function on the reflectivity and transmittance of the material surface. In the same circular aperture array structure, the wavelength selection ability is proportional to the interval distance of the array period, but the transmission peak linewidth decreases with the increase of the interval distance. The structural spectrum of the cylindrical array is closely related to the structural period. The period of the array structure increases in proportion, the center wavelengths of the reflection and transmission peak of the spectrum are red-shifted. When the height of the array structure increases proportionally, the positions of the center wavelengths of the reflection and transmission peak remain almost unchanged. When the period of the array structure increases, the center wavelength of the reflection and transmission peaks appear red-shifted, and the line width is also narrowed. For the periodic ring array structure, as the inner diameter increases, the reflection peak is significantly red-shifted, and the smaller the ring width, the faster the red-shift of the reflection peak with the wavelength. By controlling the ratio of inner diameter-to-outer diameter, the spectral characteristics of the structured surface can be effectively controlled. These simulation results provide a basis for the preparation of optical filters in the future and a new idea for the study of micro-nano characteristic structures on the surface of materials.

Detection of hypokalemia disorder and its relation with hypercalcemia in blood serum using LIBS technique for patients of colorectal cancer grade I and grade II.

Cancer continues to be the most dangerous disease around the world; it causes electrolyte imbalance as well as metabolic changes. There is a complicated relationship between electrolyte disorder and cancer. Cancer patients commonly pass with abnormalities in serum electrolyte levels such as hypokalemia, hyperkalemia, hyponatremia, and hypercalcemia. So, these electrolyte imbalances indicate the existence of paraneoplastic processes and help come to a more informed prognosis. Hypokalemia is defined as a serum potassium concentration below 3.5 mmol/L and it is the second common electrolyte imbalance seen in patients with malignant diseases. In this paper, the contribution of serum potassium concentration to tumor progression was studied by applying a promising and non-invasive technique called laser-induced breakdown spectroscopy (LIBS). It was found that there is a correlation between hypokalemia and the colorectal cancer problem. Also, significant serum potassium concentration differences were detected among two different stages of the same cancer and also between two groups of the same stage of a cancer held in common but one of them suffers from hypercalcemia. In addition, the optimum conditions of LIBS setup were arranged such that it will be suitable to work with serum samples on glass substrate.

Spectral Characteristics Simulation of Topological Micro-Nano Structures Based on Finite Difference Time Domain Method.

Natural structural colors inspire people to obtain the technology of spectral characteristics by designing and preparing micro-nano structures on the material's surface. In this paper, the finite difference time domain (FDTD) method is used to simulate the spectral selectivity of micro-nano grating on an Au surface, and the spectral response characteristics of different physical parameters to the incident light are obtained. The results show that, when the grating depth is shallow, the absorption peaks of TM polarized incident light on the material surface take on redshifts with the increase in the grating period. Meanwhile, when the depth-width ratio of the grating structure is high, the absorption peak appears in the reflection spectrum and presents a linear red shift with the increase in the grating period after the linearly polarized light TE wave incident on the surface of the micro-nano structure. At the same time, the wavelength of the absorption peak of the reflection spectrum and the grating period take on one-to-one correspondence relations, and when the TM polarized light is incident, the reflection spectrum exhibits obvious selective absorption characteristic peaks at certain grating periods (for example, when the period is 0.4 µm, there are three absorption peaks at the wavelengths of 0.7, 0.95, and 1.55 µm). These simulation results can provide a good theoretical basis for the preparation of micro-nano structures with spectral regulation function in the practical application.

LncRNA-FENDRR mediates VEGFA to promote the apoptosis of brain microvascular endothelial cells via regulating miR-126 in mice with hypertensive intracerebral hemorrhage.

BACKGROUND: LncRNA-FENDRR is a kind of endothelial genes critical for vascular development. Moreover, miR-126 and vascular endothelial growth factor A (VEGFA) are also involved in the physiological process of vascular endothelial cells. This study aimed to the underlying mechanism of FENDRR involving miR-126 and VEGFA in hypertensive intracerebral hemorrhage (HICH). METHODS: C57BL/6 mice were chosen to establish HICH model. The expression of FENDRR, miR-126, and VEGFA at mRNA level was determined by qRT-PCR. The protein expression of VEGFA was assessed using Western blot. RIP assay and RNA pull-down assay were used to the relationship between FENDRR and miR-126. Flow cytometry was used to analyze cell apoptosis. RESULTS: The levels of FENDRR and VEGFA were increased, and miR-126 expression was decreased in vascular endothelial cells (VECs) from the right brain of model mice and human brain microvascular endothelial cells (HBMECs) treated by thrombin. Overexpression of FENDRR promoted the apoptosis of HBMECs. FENDRR regulating VEGFA participated in HBMECs apoptosis through targeting miR-126. Downregulation of FENDRR was indicated to relieve the HICH in mice. CONCLUSIONS: FENDRR could promote the apoptosis of HBMECs via miR-126 regulating VEGFA in HICH.

ABT737 induces mitochondrial pathway apoptosis and mitophagy by regulating DRP1-dependent mitochondrial fission in human ovarian cancer cells.

The anti-apoptotic BCL2 family of proteins elicits a broad cell survival program mainly by promoting cell migration, invasion, and metastasis. High expression level of BCL2 family proteins is a characteristic feature of cancer cells, especially in cisplatin-resistant cancer cells. Recent studies have shown that BCL2 family proteins play a housekeeping role in modulating mitochondrial dynamics. However, it is not clear whether BCL2 family proteins are relevant to mitochondrial fission and fusion in cisplatin-resistant ovarian cancer cells. Here, we report that the BCL2/BCLXL inhibitor ABT737 induced apoptosis more potently in cisplatin-resistant SKOV3/DDP ovarian cancer cells than in cisplatin-sensitive SKOV3 ovarian cancer cells. ABT737 significantly increased levels of DRP1 in mitochondria and increased rates of mitochondrial fission, and then induced cytochrome C release from mitochondria and mitophagy in SKOV3/DDP cells. Mdivi-1, a selective inhibitor of DRP1, weakened ABT737-induced mitochondrial fission, intrinsic apoptotic pathways, and mitophagy in SKOV3/DDP cells. Taken together, these results demonstrate a novel function of ABT737 in inducing DRP1-dependent apoptotic mitochondrial fission and highlight that targeting anti-apoptotic BCL2 family proteins may be an emerging therapeutic strategy for patients with cisplatin-resistant ovarian cancer.

BMH-21 inhibits viability and induces apoptosis by p53-dependent nucleolar stress responses in SKOV3 ovarian cancer cells.

The nucleolus is a stress sensor associated with cell cycle progression and apoptosis. Studies have shown that nucleolar stress is positively correlated with apoptosis in breast, prostate and lung cancer cells. However, the role and function of nucleolar stress in ovarian cancer has not been reported. In this study, we found that the nucleolar stress inducer BMH-21 inhibited viability of SKOV3 ovarian cancer cells in a dose-dependent manner. Furthermore, BMH-21 induced the expression of nucleolar stress marker proteins (nucleolin, nucleophosmin and fibrillarin) and promoted the nuclear export of these proteins. BMH-21 also decreased MDM2 proto-oncogene expression and increased protein levels of the tumor suppressor p53 and p53 phosphorylated at serine 15 (p­p53­Ser15), which contributed to increased expression of the downstream apoptosis-related protein BCL2 associated X (BAX) and activation of caspase-3. Taken together, these data provide the first reported evidence that induction of p53-dependent nucleolar stress by BMH-21 induces apoptosis in ovarian cancer. Our data suggest that nucleolar stress might be a pathway suitable for targeting in ovarian cancer.

Increased intracellular Ca2+ decreases cisplatin resistance by regulating iNOS expression in human ovarian cancer cells.

Previous studies have reported that intracellular Ca2+ signals and inducible nitric oxide synthase (iNOS) are involved in cell apoptosis. However, the role of iNOS in cisplatin resistance in ovarian cancer remains unclear. Here, we demonstrate that SKOV3/DDP ovarian cancer cells were more resistant to cisplatin than were SKOV3 ovarian cancer cells. The expression of intracellular Ca2+ and iNOS was more strongly induced by cisplatin in SKOV3 cells than in SKOV3/DDP cells. TAT-conjugated IP3R-derived peptide (TAT-IDPS) increased cisplatin-induced iNOS expression and apoptosis in SKOV3/DDP cells. 2-Aminoethoxydiphenyl borate (2-APB) decreased cisplatin-induced iNOS expression and apoptosis in SKOV3 cells. Thus, iNOS induction may be a valuable strategy for improving the anti-tumor efficacy of cisplatin in ovarian cancer.

Subwavelength topological structures resulting from surface two-plasmon resonance by femtosecond laser exposure solid surface.

We present that surface two-plasmon resonance (STPR) in electron plasma sheet produced by a femtosecond laser irradiating a solid surface is the self-formation mechanism of periodic subwavelength ripple structures. Peaks of overdense electrons, formed by resonant two-plasmon wave mode, pull bound ions out of the metal surface. Thus, the wave pattern of STPR is "carved" on the surface by Coulomb ablation (removal) due to periodic distributed strong electrostatic field produced by charge separation. To confirm the STPR model, we have performed analogical carving experiments by two femtosecond laser beams with perpendicular polarizations and time delay. The results explicitly show that two wave patterns of STPR generated by each beam are independently created in the pulse exposure area of a target surface, which is like the traditional "layer-carving" technique by comparison with the structured topological features. The time-scale of ablation dynamics and the electron temperature in ultrafast interaction are also verified by a time-resolved spectroscopy experiment and numerical simulation, respectively. The present model can self-consistently explain the formation of subwavelength ripple structures even with spatial periods shorter than half of the laser wavelength, shedding light on the understanding of ultrafast laser-solid interaction.

Failure of Elevating Calcium Induces Oxidative Stress Tolerance and Imparts Cisplatin Resistance in Ovarian Cancer Cells.

Cisplatin is a commonly used chemotherapeutic drug, used for the treatment of malignant ovarian cancer, but acquired resistance limits its application. There is therefore an overwhelming need to understand the mechanism of cisplatin resistance in ovarian cancer, that is, ovarian cancer cells are insensitive to cisplatin treatment. Here, we show that failure of elevating calcium and oxidative stress tolerance play key roles in cisplatin resistance in ovarian cancer cell lines. Cisplatin induces an increase in oxidative stress and alters intracellular Ca(2+) concentration, including cytosolic and mitochondrial Ca(2+) in cisplatin-sensitive SKOV3 cells, but not in cisplatin-resistant SKOV3/DDP cells. Cisplatin induces mitochondrial damage and triggers the mitochondrial apoptotic pathway in cisplatin-sensitive SKOV3 cells, but rarely in cisplatin-resistant SKOV3/DDP cells. Inhibition of calcium signaling attenuates cisplatin-induced oxidative stress and intracellular Ca(2+) overload in cisplatin-sensitive SKOV3 cells. Moreover, in vivo xenograft models of nude mouse, cisplatin significantly reduced the growth rates of tumors originating from SKOV3 cells, but not that of SKOV3/DDP cells. Collectively, our data indicate that failure of calcium up-regulation mediates cisplatin resistance by alleviating oxidative stress in ovarian cancer cells. Our results highlight potential therapeutic strategies to improve cisplatin resistance.

Myricetin induces apoptosis via endoplasmic reticulum stress and DNA double-strand breaks in human ovarian cancer cells.

The mechanisms underlying myricetin-induced cancer cell apoptosis remain to be elucidated. Certain previous studies have shown that myricetin induces apoptosis through the mitochondrial pathway. Apoptosis, however, can also be induced by other classical pathways, including endoplasmic reticulum (ER) stress and DNA double­strand breaks (DSBs). The aim of the present study was to assess whether these two apoptotic pathways are involved in myricetin­induced cell death in SKOV3 ovarian cancer cells. The results revealed that treatment with myricetin inhibited viability of SKOV3 cells in a dose­dependent manner. Myricetin induced nuclear chromatin condensation and fragmentation, and also upregulated the protein levels of active caspase 3 in a time­dependent manner. In addition, myricetin upregulated ER stress­associated proteins, glucose­regulated protein­78 and C/EBP homologous protein in SKOV3 cells. Phosphorylation of H2AX, a marker of DNA DSBs, was revealed to be upregulated in myricetin-treated cells. The data indicated that myricetin induces DNA DSBs and ER stress, which leads to apoptosis in SKOV3 cells.

Tolerance to endoplasmic reticulum stress mediates cisplatin resistance in human ovarian cancer cells by maintaining endoplasmic reticulum and mitochondrial homeostasis.

The mechanism of cisplatin resistance in ovarian cancer is not fully understood. In the present study, we showed a critical role for endoplasmic reticulum (ER) stress tolerance in mediating cisplatin resistance in human ovarian cancer cells. We found cisplatin to inhibit the proliferation of two ovarian cancer cell lines: cisplatin-sensitive SKOV3 cells and cisplatin­resistant SKOV3/DDP cells. However, the effect was greater in the cisplatin-sensitive SKOV3 cells. Cisplatin treatment induced ER stress in the SKOV3 cells but not in the SKOV3/DDP cells. Cisplatin-induced Ca2+ flow from the ER into mitochondria caused mitochondrial calcium overload, which amplified proapoptotic signaling in the cisplatin-sensitive SKOV3 cells. ER stress-mediated apoptosis and mitochondrial pathway-dependent apoptosis were induced in the cisplatin-sensitive SKOV3 cells, but not in the cisplatin-resistant SKOV3/DDP cells. Moreover, there were more ER-mitochondria contacts in the cisplatin-treated SKOV3 cells. Collectively, our data indicated that tolerance to cisplatin-induced ER stress inhibits ER stress-mediated apoptosis, prevents an imbalance in ER and mitochondrial calcium homeostasis and maintains cell survival, thus leading to cisplatin resistance in ovarian cancer cells.

2-Deoxy-d-Glucose Sensitizes Human Ovarian Cancer Cells to Cisplatin by Increasing ER Stress and Decreasing ATP Stores in Acidic Vesicles.

Cisplatin is a commonly used chemotherapeutic agent; however, the development of acquired resistance limits its application. Here, we demonstrate that 2-deoxy-d-glucose (2-DG) enhanced the antitumor effects of cisplatin in SKOV3 cells, which include inhibition of proliferation and promotion of apoptosis. Additionally, either cisplatin or 2-DG alone could upregulate the endoplasmic reticulum (ER) stress-associated protein glucose-regulated protein-78 (GRP78). Moreover, exposure to 2-DG increased the expression of GRP78 induced by cisplatin. Cisplatin also upregulated ER stress-associated apoptotic protein 153/C/EBP homology protein (CHOP) in SKOV3 cells. While treatment with 2-DG alone could not upregulate the CHOP expression, a combination of both 2-DG and cisplatin increased the protein levels of CHOP above those induced by Cisplatin alone. Finally, cisplatin mediated an increase in ATP stores within acidic vesicles, whereas 2-DG decreased this effect. These data demonstrate that 2-DG sensitizes SKOV3 cells to cisplatin by increasing ER stress and decreasing ATP stores in acidic vesicles.

Proteasome inhibitor lactacystin enhances cisplatin cytotoxicity by increasing endoplasmic reticulum stress-associated apoptosis in HeLa cells.

Cisplatin is commonly used as a therapeutic agent, despite its known adverse side effects and the occurrence of drug resistance. The development of novel methods for combination therapy with cisplatin is required in order to circumvent these limitations of cisplatin alone. The proteasome inhibitor lactacystin (LAC) has been indicated to produce anti-tumor effects, and has previously been used as an antitumor agent in cancer treatment research; however, its effects in combination with cisplatin treatment are unknown. In the current study, the effects of LAC in combination with cisplatin treatment were investigated in HeLa human cervical cancer (HCC) cells. The results demonstrated that cisplatin treatment inhibited cell growth and induced cell apoptosis. HeLa cell exposure to cisplatin induced endoplasmic reticulum (ER) stress-associated apoptosis, and LAC treatment increased levels of cell apoptosis and the activation of caspase-3. Specifically, LAC treatment increased the cisplatin-induced expression of PDI, GRP78, CHOP, cleaved caspase-4 and cleaved caspase-3. Together, these data indicate that LAC is able to enhance cisplatin cytotoxicity by increasing ER stress-associated apoptosis in HeLa cells.

[Effect of flavonoids from Sophora flavescens in aging mice induced by D-galactos].

To investigate the effect of flavonoids from Sophora flavescens in aging mice induced by D-galactose and its mechanism. Totally 60 mice were randomly divided into six groups: the control group, the model group, the piracetam group (positive control group) and flavonoids from S. flavescens low, medium and high doses groups. Except for the control group, all of the rest groups were subcutaneously injected with D-galactose (160 mg x kg(-1)) for successively 30 days to establish the sub-acute senescent model. Meanwhile, flavonoids from S. flavescens low, medium and high doses groups were respectively administered with 150, 300 and 600 mg xkg-('1)of flavonoids from S. flavescens for 30 days. The learning and memory abilities of mice were determined by avoiding darkness ex-eriment and jumping stair experiment. The contents of malondialdehyde (MDA) tumor necrosis factor-aα NF-aα the activities of superoxide dismutase (SOD) monoamine oxidase-B (MAO-B) Na'(+)K'(+)-ATPase and Ca2(+ )-ATPase in the brain of mice were deter-ined respectively after the behavioral experiments. The activity of lactic dehydrogenase ( DH) in blood serum was also determined and analyzed by microscope after HE staining to observe the changes in hippocampal organizational structure. Compared with the model group, flavonoids from S. favescens medium and high doses groups showed significantly increases in the latency of avoiding darkness and jumping stair experiments; flavonoids from S. fllvescens low, medium and high doses groups and the piracetam group showed de-reases in the numbers of errors in avoiding darkness experiment; the flavonoids from S. flavescens high dose group and the piracetam group showed reduction- n the number of errors in jumping stair experiment (P <0 . 5 or P <0 . 1). Flavonoids from S. flavescens me-ium and high doses groups and the piracetam group showed improvements in the activities of SOD, Na'(+)K'(+)ATPase in the brain of mice and declines in the contents of MDA and TNF-aα the activity of MAO-B in the brain of mice, the activity of LDH in blood serum (P <0 . 5 or P <0 . 1). Flavonoids from S. flavescens low, medium and high doses groups and the piracetam group also showed im-rovement in the activity of Ca2(+ )ATPase, with statistical difference from the model group (P <0 . 5 or P <0 . 1). The pathological result showed decreases in the number of cells of hippocampal dentate gyrus area, sparse cell arrangement, incomplete cellular mor-hology, scarce cytoplasm, blurred boundary between nucleus and cytoplasm, nuclei anachromasis, irregular pyknosis and unconspicu-us nucleoli in the model group. Compared with the model group, flavonoids from S. flavescens low, medium and high doses groups and the piracetam group showed improvements in hippocampal organization tissues. Flavonoids from S. favescens can improve the learning and memory ability of senescent mice induced by D-galactose. Its mechanism may be correlated with the enhancement of anti-oxidative actions by lowering TNF-aαcontent, which results in the stability of cell membrane and the reduction in MAO-B activity.

Ammonium chloride enhances cisplatin cytotoxicity through DNA double-strand breaks in human cervical cancer cells.

Cisplatin (cis-diamminedichloroplatinum II, CDDP) acts as a therapeutic agent by initiating cellular apoptosis. However, side-effects and drug resistance limit the clinical use of cisplatin. Numerous studies have focused on the drug-target interactions, cellular pharmacology and pharmacokinetics of cisplatin. Newly developed treatment strategies are needed in order to be used in combination with cisplatin, with the aim to minimize toxicity and to circumvent cisplatin resistance. Ammonium chloride (NH4Cl) is widely used in various areas, but its use as a combination agent with cisplatin for the treatment of cancer cells has not been previously reported. In the present study, we showed that NH4Cl could be potentially used as an effective agent in cisplatin combination treatment of HeLa human cervical cancer (HCC) cells. Cisplatin was found to inhibit cell growth, as well as to induce cell apoptosis and DNA double-strand breaks. In addition, treatment with NH4Cl increased the rate of cell apoptosis and the activation of caspase-3. Particularly, we found that NH4Cl treatment increased cisplatin­induced phosphorylation of H2AX. In conclusion, our data indicate that NH4Cl enhances cisplatin cytotoxicity through increased DNA damage in HeLa HCC cells.

A modified rate equation for the propagation of a femtosecond laser pulse in field-ionizing medium.

A recombination rate of electron-ion in the strong-field atomic process is phenomenologically introduced into the ionization rate equation, and therefrom an ionization and recombination rates equation (IRRE) is obtained. By using the extended IRRE, the propagation equation of an intense femtosecond laser pulse in the gaseous medium is re-derived. Some new physical behaviors and characteristics caused by the introduced recombination rate are discussed in detail.

[Effects of schizandrins on learning-memory disorder in mice].

OBJECTIVE: To observe the effects of schizandrins on the learning and memory disorder in mice, and explore its mechanism. METHOD: The memory impairment model was established by using the pentobarbital sodium (20 mg x kg(-1)) intraperitoneally injected in mice. Schizandrins (0.5, 1.0, 2.0 g x kg(-1)) were administered through intragavage for consecutive 14 days. Morris Water Maze test was used to evaluate the impairment of learning and memory. The energy of superoxide dismutase (SOD), nitric oxide (NO) and catalase (CAT) of brain tissue were measured. And the positive expression of nuclear transcription factor-kappaB p65 (NF-kappaB p65), caspase-3 in the hippocampus CA1 region were determined by immunohistochemical analysis. At the cellular level, 24 h after schizandrins (0.062 5, 0.125, 0.25 g x L(-1)) were pre-administered, the apoptosis model of PC12 cell was induced by H2O2, and activity of PC12 cell was detected by MTT colorimetric assay, the energy of NO in cell serum were measured. The expression of Bcl-2 was determined by the combination of immunocytochemical staining and image analysis software. RESULT: Morris Water Maze test showed that the model group mice took shorter searching time and distance on the previous flat area than those in the control group (P < 0.05), which could be prolonged after schizandrins treatment (P < 0.05, P < 0.01). Compared with the control group, the level of NO increased while the activity of SOD, CAT decreased in the model group (both P < 0.01). After treated with schizandrins, the level of NO significantly decreased (P < 0.01), while the activity of SOD increased (P < 0.01). Immunohistochemistry analysis showed that the protein expression of NF-kappaB p65, Caspase-3 in the hippocampal CA1 region significantly increased after modeling, while schizandrins (1.0 g x kg(-1)) can significantly inhibit the protein expression of NF-kappaB p65, Caspase-3 (P < 0.05, P < 0.01). Compared with the H2O2, model group, schizandrins (0.125, 0.25 g x L(-1)) can significantly increased PC12 cell activity and decreased the NO level (P < 0.05, P < 0.01), the expression of Bcl-2 in the schizandrins group (0.125, 0.25 g x L(-1)) was up-regulated. CONCLUSION: Schizandrins could improve the learning-memory dysfunction induced by the sodium pentobarbital in mice, and its protective mechanism is related to the lowering oxidative damage and inhibiting the cell apoptosis through up-regulating the expression of Bcl-2.