An antifouling electrochemical biosensor based on chondroitin sulfate-functionalized polyaniline and DNA-peptide conjugates for cortisol determination in body fluids.

An antifouling electrochemical biosensor was constructed based on chondroitin sulfate (CS)-functionalized polyaniline (CS/PANI) and DNA-peptide conjugates that is capable of assaying cortisol directly in human fluids. First, a CS-doped PANI nanocomposite (sensing substrate) was electrodeposited onto a bare glassy carbon electrode to promote electron transport, providing the sensing signal from high peak currents of PANI to improve the sensitivity of the biosensor. Dendritic DNA-peptide conjugates were assembled onto the CS/PANI by exploiting the highly specific and strong interactions between biotin and streptavidin, which amplified the sensing signals toward cortisol. The integration of the DNA-peptide conjugates into the CS/PANI nanocomposite ensured that the biosensor had a synergistic antifouling effect and was capable of detecting cortisol directly in body fluids (sweat, saliva, and tears). When assaying cortisol levels, the biosensor exhibited a linear range over the cortisol concentrations of 1 × 10-12-1 × 10-7 M and a low limit of detection (0.333 × 10-12 M). In the detection of cortisol in real samples, the relative standard deviation (RSD) of the biological samples ranged from 2.94 to 4.23%, and the recovery were calculated to be in the range 95.2-103.2%.

Targeting histone deacetylase-3 blocked epithelial-mesenchymal plasticity and metastatic dissemination in gastric cancer.

BACKGROUND AND PURPOSE: Histone deacetylase (HDAC) inhibitors (HDIs) can modulate the epithelial-mesenchymal transition (EMT) progression and inhibit the migration and invasion of cancer cells. Emerging as a novel class of anti-cancer drugs, HDIs are attracted much attention in the field of drug discovery. This study aimed to discern the underlying mechanisms of Honokiol in preventing the metastatic dissemination of gastric cancer cells by inhibiting HDAC3 activity/expression. EXPERIMENTAL APPROACH: Clinical pathological analysis was performed to determine the relationship between HDAC3 and tumor progression. The effects of Honokiol on pharmacological characterization, functional, transcriptional activities, organelle structure changes, and molecular signaling were analyzed using binding assays, differential scanning calorimetry, luciferase reporter assay, HDAC3 activity, ER stress response element activity, transmission electron microscopy, immune-blotting, and Wnt/ß-catenin activity assays. The in vivo effects of Honokiol on peritoneal dissemination were determined by a mouse model and detected by PET/CT tomography. KEY RESULTS: HDAC3 over-expression was correlated with poor prognosis. Honokiol significantly abolished HDAC3 activity (Y298) via inhibition of NFκBp65/CEBPß signaling, which could be reversed by the over-expression of plasmids of NFκBp65/CEBPß. Treatments with 4-phenylbutyric acid (a chemical chaperone) and calpain-2 gene silencing inhibited Honokiol-inhibited NFκBp65/CEBPß activation. Honokiol increased ER stress markers and inhibited EMT-associated epithelial markers, but decreased Wnt/ß-catenin activity. Suppression of HDAC3 by both Honokiol and HDAC3 gene silencing decreased cell migration and invasion in vitro and metastasis in vivo. CONCLUSIONS AND IMPLICATIONS: Honokiol acts by suppressing HDAC3-mediated EMT and metastatic signaling. By prohibiting HDAC3, metastatic dissemination of gastric cancer may be blocked. Conceptual model showing the working hypothesis on the interaction among Honokiol, HDAC3, and ER stress in the peritoneal dissemination of gastric cancer. Honokiol targeting HDAC3 by ER stress cascade and mitigating the peritoneal spread of gastric cancer. Honokiol-induced ER stress-activated calpain activity targeted HDAC3 and blocked Tyr298 phosphorylation, subsequently blocked cooperating with EMT transcription factors and cancer progression. The present study provides evidence to demonstrate that HDAC3 is a positive regulator of EMT and metastatic growth of gastric cancer cells. The findings here imply that overexpressed HDAC3 is a potential therapeutic target for honokiol to reverse EMT and prevent gastric cancer migration, invasion, and metastatic dissemination. • Honokiol significantly abolished HDAC3 activity on catalytic tyrosine 298 residue site. In addition, Honokiol-induced ER stress markedly inhibited HDAC3 expression via inhibition of NFκBp65/CEBPß signaling. • HDAC3, which is a positive regulator of metastatic gastric cancer cell growth, can be significantly inhibited by Honokiol. • Opportunities for HDAC3 inhibition may be a potential therapeutic target for preventing gastric cancer metastatic dissemination.

Demulsification of oily wastewater using a nano carbon black modified with polyethyleneimine.

In this work, nano carbon black was modified with polyethyleneimine (CB-PEI) under an ultrasonic field. The obtained product was used as a demulsifier to break oily wastewater. Morphology, structure, and chemical composition of CB-PEI were systematically analyzed. Bottle test was carried out to evaluate the influence of dosage, pH value and salinity on the demulsification efficiency of the emulsion. The results showed that the light transmittance of water phase (TSW) after the demulsification was 79.1% and corresponding oil removal rate (ORR) could reach up to 99.4% with 60 mg/L of CB-PEI at ambient temperature for 30 min. In addition, the possible demulsification mechanism was explored by dynamic interface tension (IFT), elasticity modulus, wettability, self-assemble of interfacial membrane, zeta potential and micrograph analysis. It indicated that CB-PEI had an appropriate amphiphilicity and good interfacial activity, which could improve it quickly transfer to the oil-water interface and result in the oil-water separation. The current work provides a simple method to prepare a demulsifier with excellent performance, so it has a good application prospect for the treatment of oil-water emulsions.

Demulsification of water-in-crude oil emulsion driven by a carbonaceous demulsifier from natural rice husks.

Removing emulsified water from a water-in-crude oil (W/O) emulsion is critically required prior to downstream processing in the petroleum industry. In this work, environmentally friendly and amphipathic rice husk carbon (RHC) demulsifier was prepared by a simple carbonization process in a muffle furnace using rice husks as starting materials. RHC was characterized by field-emission scanning electron microscope, energy dispersive spectrometer, Fourier transform infrared spectrometer, ultraviolet-visible spectrometer, powder X-ray diffraction, zeta potential and synchronal thermal analyzer. The factors such as dosage, temperature, settling time, pH value and salinity were systematically investigated. The results indicated that the dehydration efficiency (DE) reached as high as 96.99% with 600 mg/L of RHC for 80 min at 70 °C. RHC exhibited an optimal DE under neutral condition, but it was also effective under acidic and alkaline conditions. Also, it had an excellent salt tolerance. The possible demulsification mechanism was explored by interfacial properties, different treatment methods for RHC and microexamination. The demulsification of RHC is attributed to its high interfacial activity, oxygen-containing groups and content of silica. It indicates that RHC is an effective demulsifier for the treatment of the W/O emulsion.

The pattern of alternative splicing in lung adenocarcinoma shows novel events correlated with tumorigenesis and immune microenvironment.

Lung adenocarcinoma (LUAD) is the leading cause of cancer deaths worldwide due to the lack of early diagnostic markers and specific drugs. Previous studies have shown the association of LUAD growth with aberrant alternative splicing (AS). Herein, clinical data of 535 tumor tissues and 59 normal tissues were extracted from The Cancer Genome Atlas (TCGA) database. Each sample was analyzed using the ESTIMATE algorithm; a comparison between higher and lower score groups (stromal or immune) was made to determine the overall- and progression-free survival-related differentially expressed AS (DEAS) events. We then performed unsupervised clustering of these DEASs, followed by determining their relationship with survival rate, immune cells, and the tumor microenvironment (TME). Next, two prognostic signatures were developed using bioinformatics tools to explore the prognosis of cases with LUAD. Five OS- and six PFS-associated DEAS events were implemented to establish a prognostic risk score model. When compared to the high-risk group (HRG), the PFS and OS of the low-risk group (LRG) were found to be considerable. Additionally, a better prognosis was found considerably associated with the ESTIMATE score of the patients as well as immune cells infiltration. Our analysis of AS events in LUAD not only helps to clarify the tumorigenesis mechanism of AS but also provides ideas for revealing potential prognostic biomarkers and therapeutic targets.

Nano-Particulated Erlotinib Compound System in Alleviation of Lung Cancer.

To produce an effective nanoparticle-loaded delivery system for the tumor drug erlotinib for non-small cell lung cancer (NSCLC) therapy, we loaded poly(lactic co glycolic acid) (PLGA) nanoparticles with erlotinib and used them to transport the drug to a target area. NCI-H1650 cells were cultured to test the permeability, efficiency, and anti-tumor capacity of PLGA and polyethyleneimine (PEI) drug delivery systems, and an NSCLC mouse model was prepared to further test the anti-tumor efficiency of PLGA. In tests using NCI-H1650 cells, we found that PLGA could effectively transport erlotinib into tumor cells, and release the loaded drug instantly. The infiltration efficiency was significantly higher than that of the PEI delivery system, and the same results were obtained in animal tests. PLGA-erlotinib could promote apoptosis and inhibit the migration of tumor cells more effectively than PEI-erlotinib. In the NSCLC mouse model, PLGA could more effectively reduce the tumor volume and the extent of tumor markers than the PEI delivery system. Immune function was also better rescued with the use of the PLGA system. We concluded that PLGA-erlotinib may be a good choice for lung cancer therapy in the future.

miRNA-Based Potential Biomarkers and New Molecular Insights in Ulcerative Colitis.

Ulcerative colitis (UC) is a chronic non-specific inflammatory bowel disease, which usually manifests as abdominal pain, diarrhea and hematochezia. The disease often recurs and is difficult to cure. At present, the pathogenesis is not clear, but it is believed that the disease is caused by a complex interaction among immunity, heredity, environment and intestinal microflora disorders. MicroRNA (miRNA) is endogenous single-stranded non-coding RNA of 17-25 nucleotides (nts). They target the 3'Untranslated Region of a target gene and inhibit or degrade the target gene according to the extent of complementary bases. As important gene expression regulators, miRNAs are involved in regulating the expression of most human genes, and play an important role in the pathogenesis of many autoimmune diseases including UC. Studies in recent years have illustrated that abnormal expression of miRNA occurs very early in disease pathogenesis. Moreover, this abnormal expression is highly related to disease activity of UC and colitis-associated cancer, and involves virtually all key UC-related mechanisms, such as immunity and intestinal microbiota dysregulation. Recently, it was discovered that miRNA is highly stable outside the cell in the form of microvesicles, exosomes or apoptotic vesicles, which raises the possibility that miRNA may serve as a novel diagnostic marker for UC. In this review, we summarize the biosynthetic pathway and the function of miRNA, and summarize the usefulness of miRNA for diagnosis, monitoring and prognosis of UC. Then, we described four types of miRNAs involved in regulating the mechanisms of UC occurrence and development: 1) miRNAs are involved in regulating immune cells; 2) affect the intestinal epithelial cells barrier; 3) regulate the homeostasis between gut microbiota and the host; and 4) participate in the formation of tumor in UC. Altogether, we aim to emphasize the close relationship between miRNA and UC as well as to propose that the field has value for developing potential biomarkers as well as therapeutic targets for UC.

Nanoscale silica-coated graphene oxide and its demulsifying performance in water-in-oil and oil-in-water emulsions.

In current work, GO@SiO2 nanocomposite was prepared by coating nanoscale silica onto graphene oxide (GO). GO@SiO2 was characterized with scanning electron microscopy (SEM), X-ray diffraction (XRD), and Fourier-transform infrared spectroscopy (IF-IR). Additionally, the demulsifying performance of GO@SiO2 was investigated by bottle test. The results showed that GO@SiO2 had a good demulsifying performance in both oil-in-water (O/W) and water-in-oil (W/O) emulsions. When the concentration of GO@SiO2 was 200 ppm in the O/W emulsion, the optimal light transmittance of aqueous phase (LTA) and corresponding oil removal rate (ORR) at room temperature could reach 86.9% and 99.48%, respectively. Also, GO@SiO2 had an excellent salt tolerance under acidic condition. Furthermore, GO@SiO2 also could demulsify the W/O emulsion, and the efficiency at 70 °C could reach 80.5% when the concentration was 400 ppm.

E2F2 inhibition induces autophagy via the PI3K/Akt/mTOR pathway in gastric cancer.

BACKGROUND: E2F2 is a member of the E2F transcription factor family and has important but not fully understood biological functions in cancers. The biological role of E2F2 in gastric cancer (GC) also remains unclear. METHODS: We examined the expression levels of E2F2 in GC using publicly available datasets such as TIMER, Oncomine, GEPIA, UALCAN, etc., and in our patient cohort, using quantitative real-time PCR, western blotting, and immunohistochemistry. We further investigated the effects of E2F2 on phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling, autophagy, and the migration and invasion of GC cells by the wound healing assay, Transwell assay and transmission electron microscopy. RESULTS: E2F2 was highly expressed in both GC tissues and cells compared with normal gastric tissues/cells. High E2F2 expression was associated with poor overall survival (OS). In addition, the expression of E2F2 in GC was strongly correlated with a variety of immune markers. E2F2 overexpression promoted the migration and invasiveness of GC cells in vitro through inhibition of PI3K/Akt/mTOR-mediated autophagy. CONCLUSION: High E2F2 expression was associated with the characteristics of invasive tumors and poor prognosis. E2F2 also had potential modulatory effects on tumor immunity. We discovered a novel function of E2F2 in the regulation of PI3K/Akt/mTOR-mediated autophagy and the downstream processes of cell migration and invasion.

Expression and function of transmembrane 4 superfamily proteins in digestive system cancers.

BACKGROUND: Although the medical level is constantly improving, cancer is still a major disease that threatens human health, and very effective treatments have not been found. In recent years, studies have found that four-transmembrane superfamily proteins are involved in multiple stages of tumorigenesis and development, but their expression and function in tumors have not been systematically studied. METHODS: We used the Oncomine database to analyze the mRNA expression levels of TSPAN family in various cancers. Then differentially expressed genes were screened out and verified by liver cancer, colorectal cancer, and gastric cancer cells by q-PCR and Western blot analysis. CCK8 and EDU analysis are used to detect cell proliferation, Cell wound scrape assay and Cell invasion assay are used to analyze cell invasion and metastasis. Nude tumor formation test used to verify the tumor suppressive effect of TSPAN7 in vivo. RESULTS: Differential analysis of 33 TSPAN proteins revealed that a total of 11 proteins showed differential expression in 10% of independent analyses, namely TSPAN1, TSPAN3, TSPAN5, TSPAN6, TSPAN7, TSPAN8, TSPAN13, TSPAN25, TSPAN26, TSPAN29, TSPAN30. TSPAN7 is the only four-transmembrane protein with reduced expression in three types of digestive tract tumors, so we chose TSPAN7 to be selected for cellular and molecular level verification. We found that compared with normal cells, the expression of TSPAN7 in liver cancer cells was significantly reduced, while the expression of gastric and colon cancer was not significantly different from that of normal cells. In addition, we also found that the high expression of Tspan7 not only inhibited the proliferation of HCC-LM3 cells, but also inhibited its invasion and metastasis. CONCLUSIONS: Our study evaluated the expression and function of the TSPANs family in digestive cancers and explored TSPAN7 in hepatoma cells in detail. We found some members of the TSPAN family show significant expression differences between cancer and normal tissues, of which TSPAN7 may be a potential biomarker for liver cancer.

Lactational changes of fatty acids and fat-soluble antioxidants in human milk from healthy Chinese mothers.

Human milk fat is specially tailored to supply the developing infant with adequate and balanced nutrients. The present study aimed to quantify the composition of fatty acids, tocopherols and carotenoids in human milk, with special emphasis on the lactational changes. Colostrum, transitional and mature milk samples were collected longitudinally from the same forty-two healthy, well-nourished Chinese mothers. Fatty acids were quantified by GC with carotenoids (carotenes and xanthophylls) and tocopherols (α-, γ-tocopherol) determined by HPLC. Total fatty acid (TFA) content increased from 15·09 g/l in colostrum to 32·57 g/l in mature milk with the percentages of DHA and arachidonic acid (ARA) decreased. The ratio of n-6:n-3 PUFA and ARA:DHA remained constant during lactation at about 11:1 and 1·3:1, respectively. Both α-tocopherol and γ-tocopherol decreased over lactation with the ratio of α-:γ-tocopherol declined significantly from 7·21:1 to 4·21:1 (P < 0·001). Carotenoids all dropped from colostrum to mature milk as the less polar carotenes dropped by 88·67 %, while xanthophylls only dropped by 35·92 %. Lutein was predominated in both transitional and mature milk carotenoids (51·64-52·49 %), while colostrum carotenoids were mainly composed of lycopene (32·83 %) and ß-carotene (30·78 %). The concentrations of tocopherols and xanthophylls but not carotenes were positively associated with TFA content in milk. These results suggested that colostrum and mature milk contained divergent lipid profiles and selective transfer mechanisms related to polarity might be involved. The present outcomes provide new insights for future breast-feeding studies, which also add in scientific evidences for the design of both initial and follow-on infant formulas.

Dietary Choline Intake during Pregnancy and PEMT rs7946 Polymorphism on Risk of Preterm Birth: A Case-Control Study.

INTRODUCTION AND AIMS: Choline-metabolizing genetic variation may interact with choline intake on fetal programming and pregnancy outcome. This case-control study aims to explore the association of maternal choline consumption and phosphatidylethanolamine N-methyltransferase (PEMT) gene polymorphism rs7946 with preterm birth risk. METHODS: 145 Han Chinese women with preterm delivery and 157 Han Chinese women with term delivery were recruited in Shanghai. Dietary choline intake during pregnancy was assessed using a validated food frequency questionnaire. Additionally, DNA samples were genotyped for PEMT rs7946 (G5465A) with plasma homocysteine (Hcy) levels measured. RESULTS: Compared with the lowest quartile of choline intake, women within the highest consumption quartile had adjusted odds ratio (aOR) for preterm birth of 0.48 (95% confidence interval, CI [0.24, 0.95]). There was a significant interaction between maternal choline intake and PEMT rs7946 (p for interaction = 0.04), where the AA genotype carriers who consumed the energy-adjusted choline <255.01 mg/day had aOR for preterm birth of 3.75 (95% CI [1.24, 11.35]), compared to those with GG genotype and choline intake >255.01 mg/day during pregnancy. Additionally, the greatest elevated plasma Hcy was found in the cases with AA genotype and choline consumption <255.01 mg/day (p < 0.001). CONCLUSION: The AA genotype of PEMT rs7946 may be associated with increased preterm birth in these Han Chinese women with low choline intake during pregnancy.

Posterior reversible encephalopathy syndrome after postpartum hemorrhage and uterine artery embolization: A case report.

RATIONALE: Posterior reversible encephalopathy syndrome (PRES) is characterized by clinical and radiological features, including headache, disturbed consciousness, seizures, and cortical blindness associated with findings indicating posterior leukoencephalopathy on imaging studies. Ours is the first case of PRES developing after postpartum hemorrhage and uterine artery embolization. PATIENT CONCERNS: An 18-year-old patient had postpartum hemorrhage after a normal delivery. She required uterine artery embolization to stop the bleeding; however, she developed PRES 2 hours after the surgery. DIAGNOSES: Brain computed tomography suggested subarachnoid hemorrhage or cerebral venous sinus thrombosis. However, findings on magnetic resonance imaging were highly indicative of PRES. INTERVENTIONS: The patient received diazepam and midazolam to prevent seizures. OUTCOMES: Seizures were controlled on the first day. The patient's visual acuity returned to normal on the fourth day of admission. Thirteen days after admission, her neurological signs and symptoms were completely managed. LESSONS: PRES may be related to postpartum hemorrhage, blood pressure fluctuation, inflammation, and contrast agents. Collectively, they cause a breakage in the blood-brain barrier and endothelial cell damage, eventually leading to PRES. We also found PRES had many features similar with contrast-induced encephalopathy.

Immature monocytes contribute to cardiopulmonary bypass-induced acute lung injury by generating inflammatory descendants.

BACKGROUND: As immune regulatory and effector cells, monocytes play an important role in the blood-extracorporeal circuit contact-related acute lung injury in patients undergoing cardiopulmonary bypass (CPB). However, circulating monocytes are phenotypically and functionally heterogeneous, so we characterised how immature monocytes affect acute lung injury induced by CPB. METHODS: The identification and dynamic changes in monocyte subsets were monitored by flow cytometry in patients undergoing CPB and in a rat model of CPB. The differentiation and migration of monocyte subsets were explored by in vitro cultures and adoptive transfer in the CPB rat model. RESULTS: We observed a dramatic increase of two monocyte subsets in the peripheral blood of patients undergoing CPB, involving tumour necrosis factor (TNF)-α-producing, mature intermediate CD14highCD16+ monocytes and a novel immature CD14lowCD16- subset. The immature CD14lowCD16- monocytes possessed limited ability for TNF-α production, and failed to suppress T-cell proliferation mediated by T-cell receptor signalling. However, these immature cells were highly proliferative and could differentiate into TNF-α producing, mature CD14highCD16+ monocytes. In the rat model of CPB, we further demonstrated that CPB induced migration of immature monocytes into the lungs, either from the bone marrow or from the spleen. Moreover, we confirmed the hypothesis that immature subsets could contribute to CPB-induced acute lung injury by giving rise to TNF-α producing descendants. CONCLUSIONS: The immature CD14lowCD16- monocytes might contribute to blood-circuit contact-induced acute lung injury by generating TNF-α-producing, mature monocytes. New strategies based on monocyte manipulation could be a promising therapeutic approach for minimising CPB-related lung injury.

Clinical profile of Parkinson's disease in the Gumei community of Minhang district, Shanghai

OBJECTIVE: We examined the demographic and clinical profiles of Parkinson's disease in Shanghai, China, to assist in disease management and provide comparative data on Parkinson's disease prevalence, phenotype, and progression among different regions and ethnic groups. METHODS: A door-to-door survey and follow-up clinical examinations identified 180 community-dwelling Han-Chinese Parkinson's disease patients (104 males, 76 females). RESULTS: The average age at onset was 65.16±9.60 years. The most common initial symptom was tremor (112 patients, 62.22%), followed by rigidity (38, 21.11%), bradykinesia (28, 15.56%) and tremor plus rigidity (2, 1.11%). Tremor as the initial symptom usually began in a single limb (83.04% of patients). The average duration from onset to mild Parkinson's disease (Hoehn-Yahr phase 1-2) was 52.74±45.64 months. Progression from mild to moderate/severe Parkinson's disease (phase≥3) was significantly slower (87.07±58.72 months; p<0.001), except for patients presenting initially with bradykinesia (53.83±24.49 months). Most patients (149/180, 82.78%) took levodopa with or without other drugs. The Hamilton Anxiety Scale revealed symptoms of clinical anxiety in 35 patients, and the Hamilton Depression Scale revealed depressive symptoms in 88 patients. The depressed or anxious subgroup (123 patients) demonstrated a significantly younger age at onset (55.54±7.68 years) compared with the overall mean (p<0.05). CONCLUSION: Unilateral limb tremor was the most common initial symptom, and motor function deteriorated slowly over ≅4−9 years. Earlier-onset patients experience greater psychiatric dysfunction. .

Protection against neurotoxicity by an autophagic mechanism

The objective of the present study was to investigate the effects of 3-n-butylphthalide (NBP) on a 1-methyl-4-phenylpyridinium (MPP+)-induced cellular model of Parkinson’s disease (PD) and to illustrate the potential mechanism of autophagy in this process. For this purpose, rat PC12 pheochromocytoma cells were treated with MPP+ (1 mM) for 24 h following pretreatment with NBP (0.1 mM). Cell metabolic viability was determined by the MTT assay and cell ultrastructure was examined by transmission electron microscopy. The intracellular distribution and expression of α-synuclein and microtubule-associated protein light chain 3 (LC3) were detected by immunocytochemistry and Western blotting. Our results demonstrated that: 1) NBP prevented MPP+-induced cytotoxicity in PC12 cells by promoting metabolic viability. 2) NBP induced the accumulation of autophagosomes in MPP+-treated PC12 cells. 3) Further study of the molecular mechanism demonstrated that NBP enhanced the colocalization of α-synuclein and LC3 and up-regulated the protein level of LC3-II. These results demonstrate that NBP protects PC12 cells against MPP+-induced neurotoxicity by activating autophagy-mediated α-synuclein degradation, implying that it may be a potential effective therapeutic agent for the treatment of PD.

Protection against neurotoxicity by an autophagic mechanism.

The objective of the present study was to investigate the effects of 3-n-butylphthalide (NBP) on a 1-methyl-4-phenylpyridinium (MPP+)-induced cellular model of Parkinson's disease (PD) and to illustrate the potential mechanism of autophagy in this process. For this purpose, rat PC12 pheochromocytoma cells were treated with MPP+ (1 mM) for 24 h following pretreatment with NBP (0.1 mM). Cell metabolic viability was determined by the MTT assay and cell ultrastructure was examined by transmission electron microscopy. The intracellular distribution and expression of α-synuclein and microtubule-associated protein light chain 3 (LC3) were detected by immunocytochemistry and Western blotting. Our results demonstrated that: 1) NBP prevented MPP+-induced cytotoxicity in PC12 cells by promoting metabolic viability. 2) NBP induced the accumulation of autophagosomes in MPP+-treated PC12 cells. 3) Further study of the molecular mechanism demonstrated that NBP enhanced the colocalization of α-synuclein and LC3 and up-regulated the protein level of LC3-II. These results demonstrate that NBP protects PC12 cells against MPP+-induced neurotoxicity by activating autophagy-mediated α-synuclein degradation, implying that it may be a potential effective therapeutic agent for the treatment of PD.