Hierarchical zeolites containing embedded Cd0.2Zn0.8S as a photocatalyst for hydrogen production from seawater.

Uncovering an efficient and stable photocatalytic system for seawater splitting is a highly desirable but challenging goal. Herein, Cd0.2Zn0.8S@Silicalite-1 (CZS@S-1) composites, in which CZS is embedded in the hierarchical zeolite S-1, were prepared and show remarkably high activity, stability and salt resistance in seawater.

LncRNA DGUOK-AS1 facilitates non-small cell lung cancer growth and metastasis through increasing TRPM7 stability via m6A modification.

BACKGROUND: N6-methyladenosine (m6A) modification plays key roles in tumor progression. LncRNA deoxyguanosine kinase antisense RNA 1 (DGUOK-AS1) has been reported as a promoter in tumors, but its role and mechanism in non-small cell lung cancer (NSCLC) development remain uncertain. METHODS: Cell proliferation, migration, invasion and angiogenesis were investigated via CCK-8, colony formation, transwell, and tube formation assays, respectively. The location of DGUOK-AS1 was detected via FISH assay. The interaction relationship among DGUOK-AS1, IGF2BP2 and TRPM7 was confirmed by RIP and MeRIP assays. The effects of DGUOK-AS1 on NSCLC growth and metastasis in vivo were investigated using xenograft and pulmonary metastatic models. RESULTS: DGUOK-AS1 was upregulated in NSCLC. DGUOK-AS1 silencing inhibited NSCLC cell proliferation, migration, invasion and angiogenesis. DGUOK-AS1 was mostly expressed in cytoplasm, and positively regulated IGF2BP2. METTL3/IGF2BP2 axis could increase TRPM7 mRNA stability in m6A-dependent manner. TRPM7 overexpression reversed the inhibitive function of DGUOK-AS1 silencing on NSCLC development. DGUOK-AS1 knockdown suppressed NSCLC cell growth and metastasis in nude mice. CONCLUSION: DGUOK-AS1 silencing restrains NSCLC cell growth and metastasis through decreasing TRPM7 stability via regulation of the METTL3/IGF2BP2-mediated m6A modification.

Intrapleural treatment in patients with non-small cell lung cancer with malignant pleural effusions in the real world.

BACKGROUND: The aim of the study was to assess the efficacy and side-effects of intrapleural treatment in non-small cell lung cancer (NSCLC) patients with malignant pleural effusions (MPEs). METHODS: The medical records of NSCLC patients with MPEs diagnosed in four Chinese hospitals from October 2014 to December 2019 were searched. The Kaplan-Meier method is used to calculate median overall survival (MOS) and subgroup analyses are done. RESULTS: A total of 285 patients were evaluated; 81.1% of patients received intrapleural treatment, and no patients received talc pleurodesis. MOS of the whole cohort was 21 months. Patients were divided into three groups: erythromycin group (EG; intrapleural treatment with drugs and erythromycin); intrathoracic treatment group (ITG; intrapleural treatment with drugs); control group (CG; no drug treatment in the pleural cavity). The MOS of patients in the EG, ITG and CG was 20, 22, and 19 months, respectively. Among patients who received only chemotherapy as systemic therapy, the MOS of intrathoracic administration group (IAG; i.e., EG and ITG) was longer than that of CG (12 vs. 6 months; p = 0.034), and the MOS of patients with a ratio of carcinoembryonic antigen in pleural effusion (PE-CEA): CEA in blood (B-CEA) ≤1 is worse than that of patients with a ratio >1 (4 vs. 12 months, p = 0.021) and that of CG (4 vs. 6 months, p = 0.442). CONCLUSIONS: Intrapleural treatment can prolong the survival of NSCLC patients with MPE who do not receive targeted treatment or who only receive chemotherapy. The PE-CEA: B-CEA ratio can be used to predict the efficacy if intrapleural treatment is indicated.

Impairment of learning and memory induced by perinatal exposure to BPA is associated with ERα-mediated alterations of synaptic plasticity and PKC/ERK/CREB signaling pathway in offspring rats.

The effect of bisphenol A (BPA) on learning and memory has attracted much attention recently, but its underlying mechanism remains unclear. We aimed to investigate whether the impairment of learning and memory induced by perinatal exposure to BPA was associated with the hippocampal estrogen receptor α (ERα)-mediated synaptic plasticity and PKC/ERK/CREB signaling pathway in different sex offspring rats. Pregnant Sprague-Dawley rats were treated with BPA (1 and 10 µg/mL) through drinking water from gestational day (GD) 6 to postnatal day (PND) 21. After weaning, offspring drank BPA-free water until PND 56. Morris water maze, placement and object recognition, and step-down passive avoidance task were performed. The serum estradiol (E2) levels, histopathology of hippocampus, and the expression of learning and memory related proteins were measured. The results showed that spatial and recognition memory were impaired in BPA-exposed female and male offspring, but the impaired passive avoidance memory presented only in males, not in females. The serum E2 levels were increased in BPA-exposed females and males. BPA altered the morphology and quantity of hippocampal neurons. The levels of ERα, NMDA receptor subunit 2B (NR2B), p-NR2B, AMPA receptor 1 (GluA1), p-GluA1, PSD-95, synapsin I, PKC, p-ERK and p-CREB protein expression were decreased in BPA exposed females and males, and there were interactions of sex × BPA exposure in ERα, p-NR2B and p-ERK levels. These findings suggested that perinatal exposure to BPA has sex-specific effects on learning and memory, which is associated with ERα-mediated impairment of synaptic plasticity and down-regulation of PKC/ERK/CREB signaling pathway.

The imbalance of Treg/Th17 cells induced by perinatal bisphenol A exposure is associated with activation of the PI3K/Akt/mTOR signaling pathway in male offspring mice.

Bisphenol A (BPA) can inhibit the differentiation and function of regulatory T cells (Treg), and affect the balance of helper T cell (Th) 1/Th2, therefore, the immunotoxicity of BPA has attracted widespread attention in recent years, but its mechanism is not clear. The main aim of this study was to explore the regulatory mechanism of the PI3K/Akt/mTOR signaling pathway in the context of perinatal exposure to BPA-induced Treg/Th17 imbalance in male offspring mice through a combination of in vivo and in vitro methods. Our results showed that perinatal exposure to BPA could increase the number of Th17 cells while decreasing Treg cell numbers, which was consistent with the expression levels of up-regulation of RORγt protein and a down-regulation FOXP3 protein in the splenocytes of the male offspring mice. BPA could activate the PI3K/Akt/mTOR signaling pathway and increase the inflammatory response, as evidenced by higher serum IL-17 and TNF-α levels by inducing the activation of the AhR and TLR4/NF-κB signaling pathways. Moreover, our results also supported the hypothesis whereby the Treg/Th17 imbalance, induced by perinatal exposure to BPA, was associated with the activation of PI3K/Akt/mTOR signaling in vitro-cultured peripheral blood mononuclear cells by using rapamycin as an inhibitor of mTOR.

Combined Exposure to Fructose and Bisphenol A Exacerbates Abnormal Lipid Metabolism in Liver of Developmental Male Rats.

The aim of this study was to investigate whether combined exposure to fructose and bisphenol A (BPA) has a synergistic effect on abnormal lipid metabolism in the liver of developmental male rats and its possible mechanism. Fifty weaned male Wistar rats were divided into five groups: the control, 13% fructose, 20% fructose, 1 µg/mL BPA, and 13% fructose + 1 µg/mL BPA (combined exposure). Rats were exposed to fructose and/or BPA through drinking water for eight weeks. Genes or proteins regulating lipid metabolism include sterol regulatory element binding protein 1 (SREBP1), adipose triglyceride lipase (ATGL), hormone sensitive lipase (HSL), acetyl-CoA carboxylase 1 (ACC1), fatty acid synthase (FAS), zinc α 2 glycoprotein (ZAG) and estrogen receptor α (ERα), and the expression of proteins regulating inflammatory response, such as TLR4 and NF-κB, were determined. Serum total cholesterol (T-CHO), triglyceride (TG), low, high density lipoprotein cholesterol (LDL-C, HDL-C), blood glucose, insulin, IL-17 and TNF-α levels were also measured. Liver tissue morphology was observed by H&E staining. The results showed that the levels of gene and protein catalyzing lipogenesis were increased (SREBP1, ACC1 and FAS), while those catalyzing lipolysis were decreased (ATGL, HSL and ZAG), accompanied by dyslipidemia, insulin resistance and hepatic fat accumulation, and there were higher expression of TLR4 and NF-κB protein and lower expression of ERα protein in liver, and increased serum IL-17 and TNF-α levels in fructose and/or BPA exposed rats compared with controls. Moreover, the above indicators were more serious in combined exposure group than in single exposure group. Therefore, abnormal lipid metabolism in the liver of developmental rats could be exacerbated by combined exposed to fructose and BPA.

Non-alcoholic Fatty Liver Disease Induced by Perinatal Exposure to Bisphenol a Is Associated With Activated mTOR and TLR4/NF-κB Signaling Pathways in Offspring Rats.

Accumulating evidence suggests a role of bisphenol A (BPA) in non-alcoholic fatty liver disease (NAFLD), and its mechanism may be related to the up-regulation of lipogenic genes, but the mechanism of BPA induced lipogenic gene expression remains unknown. The aim of this study was to investigate the effects of perinatal exposure to BPA on NAFLD and its mechanisms. Pregnant Sprague-Dawley rats had access to drinking water containing 1 or 10 µg/ml BPA from gestational day 6 to post-natal day 21. For 5 weeks after weaning, offspring drank normal water without BPA. Body weight, lipid profile and the expression of genes or proteins involved in mTOR mediated lipid metabolism and autophagy, as well as inflammatory response were investigated in the 8-wk-old offspring of different genders. The results showed that body weight was increased only in females, however, males, and females from dams treated with BPA had significantly excess visceral adipose tissue, which was consistent with adipocyte hypertrophy. Elevated TG levels and up-regulation of lipogenic genes or proteins in liver, such as sterol regulatory element binding protein 1 (SREBP1), acetyl-CoA carboxylase 1 (ACC1), and fatty acid synthase (FAS) were consistent with increased liver lipid droplets in offspring exposed to BPA. Compared with controls, the protein levels of InsR, p-IRS-1, IRS-1, TSC1, and TSC2 were decreased, p-PI3K, p-Akt (S473), p-Akt (T308), p-mTOR, and mTOR were increased, and the impaired autophagic degradation was evidenced by increased protein levels of p62, although the levels of p-ULK1, Beclin1, and LC3B proteins were increased in liver of BPA-exposed offspring. The levels of TLR4 and NF-κB proteins were also significantly increased, and ERα protein was significantly decreased in BPA-exposed offspring. Our findings indicate that perinatal exposure to BPA causes the development of NAFLD in both female and male offspring, which is associated with up-regulation of lipogenic genes, dysregulated autophagy and activated inflammatory response involving the PI3K/Akt/mTOR and TLR4/NF-κB pathways.

The Immune Escape Mechanisms of Mycobacterium Tuberculosis.

Epidemiological data from the Center of Disease Control (CDC) and the World Health Organization (WHO) statistics in 2017 show that 10.0 million people around the world became sick with tuberculosis. Mycobacterium tuberculosis (MTB) is an intracellular parasite that mainly attacks macrophages and inhibits their apoptosis. It can become a long-term infection in humans, causing a series of pathological changes and clinical manifestations. In this review, we summarize innate immunity including the inhibition of antioxidants, the maturation and acidification of phagolysosomes and especially the apoptosis and autophagy of macrophages. Besides, we also elaborate on the adaptive immune response and the formation of granulomas. A thorough understanding of these escape mechanisms is of major importance for the prevention, diagnosis and treatment of tuberculosis.

Decreased Capacity for Sperm Production Induced by Perinatal Bisphenol A Exposure Is Associated with an Increased Inflammatory Response in the Offspring of C57BL/6 Male Mice.

Many previous studies have indicated the adverse effects of bisphenol A (BPA) on sperm production and quality; however, the mechanisms underlying BPA male reproductive toxicity have yet to be elucidated. The main purpose of this study was to investigate the effect of perinatal exposure to BPA on the spermatogenic capacity of male offspring, and to explore the possible influence of inflammatory responses in BPA reproductive toxicity. Twenty-one pregnant C57BL/6mice were randomly divided into three groups: a control group, a group receiving 0.2 µg/mL (LBPA), and a group receiving 2 µg/mL of BPA (HBPA), all via drinking water from gestational day 6 to the end of lactation. After weaning, one male mouse was randomly selected from each group (n = 7/group); these three mice were fed a normal diet and drinking water for 1 month. Levels of serum testosterone (T) and tumor necrosis factor (TNF)-α were then measured in all mice. Sperm count and the proportion of sperm malformation were also determined. The levels of Toll-like receptor 4 (TLR4), nuclear factor (NF)-κB, and aryl hydrocarbon receptor (AhR) protein expression in the testis tissue were determined. Analysis showed that the proportion of sperm malformation increased in the LBPA and HBPA groups (p < 0.05). Sperm count significantly decreased only in the HBPA group (p < 0.05), while the levels of serum TNF-α increased in the LBPA and HBPA groups (p < 0.05). Levels of serum T decreased significantly in the HBPA group, compared with controls (p < 0.05). Levels of TLR4 and NF-κB protein expression in the testis were significantly higher in the LBPA and HBPA groups (p < 0.05 or p < 0.01), while AhR protein expression was higher and seminiferous tubules in the testis showed more damage in the HBPA group compared to controls (p < 0.05 and p < 0.01, respectively). Our results showed that perinatal exposure to low or high doses of BPA decreased the capacity for spermatogenesis in male offspring, which may be associated with an inflammatory response activated by the TLR4/ NF-κB and AhR signaling pathways in the testis.

The Protective Effect of Antarctic Krill Oil on Cognitive Function by Inhibiting Oxidative Stress in the Brain of Senescence-Accelerated Prone Mouse Strain 8 (SAMP8) Mice.

Alzheimer's disease (AD) is a common neurodegenerative disorder, and oxidative stress plays a vital role in its progression. Antarctic krill oil (AKO) is rich in polyunsaturated fatty acids, which has various biological activities, such as improving insulin sensitivity, alleviating inflammation and ameliorating oxidative stress. In this study, the protective effect of AKO against AD were investigated in senescence-accelerated prone mouse strain 8 (SAMP8) mice. Results showed that treatment with AKO could effectively ameliorate learning and memory deficits and ease the anxiety in SAMP8 mice by Morris water maze, Barnes maze test and open-field test. Further analysis indicated that AKO might reduce ß-amyloid (Aß) accumulation in hippocampus through decreasing the contents of malondialdehyde (MDA) and 7,8-dihydro-8-oxoguanine (8-oxo-G), increasing the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the brain of SAMP8 mice. PRACTICAL APPLICATION: The results of Morris water maze, Barnes maze test and open-field test indicated that Antarctic krill oil (AKO) improved the cognitive function and anxiety of SAMP8 mice. AKO reduced the Aß42 level in hippocampus of SAMP8 mice. AKO ameliorated oxidative stress in brain rather than in serum and liver of SAMP8 mice.

Cerebrosides from Sea Cucumber Protect Against Oxidative Stress in SAMP8 Mice and PC12 Cells.

Alzheimer's disease (AD) is a neurodegenerative disorder. Emerging evidence implicates ß-amyloid (Aß) plays a critical role in the progression of AD. In this study, we investigated the protective effect of cerebrosides obtained from sea cucumber against senescence-accelerated mouse prone 8 (SAMP8) mice in vivo. We also studied the effect of cerebrosides on Aß-induced cytotoxicity on the rat pheochromocytoma cell (PC12) and the underlying molecular mechanisms. Cerebrosides ameliorated learning and memory deficits and the Aß accumulation in demented mice, decreased the content of malondialdehyde (MDA), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-OHdG), 8-hydroxy-2'-deoxyguanosine (8-oxo-G), and nitric oxide (NO), and enhanced the superoxide dismutase (SOD) activity significantly. The neuroprotective effect of sea cucumber cerebrosides (SCC) was also verified in vitro: the cerebrosides increased the survival rate of PC12 cells, recovered the cellular morphology, downregulated the protein levels of Caspase-9, cleaved Caspase-3, total Caspase-3, and Bax, and upregulated the protein level of Bcl-2, revealing that cerebrosides could inhibit Aß-induced cell apoptosis. The results showed the protective effect of SCC was regulated by the mitochondria-dependent apoptotic pathway. Our results provide a new approach to developing the marine organisms as functional foods for neuroprotection.

Visual Chronometric Assay for Chromium(III) Ions Based on the Cu2O Nanocube-Mediated Clock Reaction.

We report a visual chronometric assay for Cr3+ based on the Cu2O nanocube-mediated clock reaction of methylene blue (MB) and N2H4. MB with a blue color can be easily reduced by excess N2H4 to form colorless leuco-MB in the presence of Cu2O nanocubes as a catalyst in a short time. However, the addition of Cr3+ decreases the catalytic activity of Cu2O nanocubes owing to the coordination interactions between them, leading to an increase in the reaction time. The reaction time change was employed for selective detection of Cr3+. This assay has a wide dynamic range from 0.03 to 600 µM with a limit of detection of 2.7 nM. Remarkably, different concentrations of Cr3+ can be directly detected with the naked eye by observing the color-fading speed. Additionally, this assay was successfully used to determine Cr3+ in real water samples.

Efficient hydrolysis of corncob residue through cellulolytic enzymes from Trichoderma strain G26 and L-lactic acid preparation with the hydrolysate.

To prepare fermentable hydrolysate from corncob residue (CCR), Trichoderma strain G26 was cultured on medium containing CCR for production of cellulolytic enzymes through solid-state fermentation (SSF), resulting in 71.3 IU/g (FPA), 136.2 IU/g (CMCase), 85.1 IU/g (ß-glucosidase) and 11,344 IU/g (xylanase), respectively. Through a three-stage saccharification strategy, CCR was hydrolyzed by the enzymatic solution (6.5 FPU/ml) into fermentable hydrolysate containing 60.1g/l glucose (81.2% cellulose was converted at solid loading of 12.5%), 21.4% higher than that by the one-stage method. And then the hydrolysate was used to produce L-lactic acid by a previous screened strain Bacillus coagulans ZX25 in the submerged fermentation. 52.0 g/l L-lactic acid was obtained after fermentation for 44 h, with 86.5% glucose being converted to L-lactic acid. The results indicate that the strains and the hydrolysis strategy are promising for commercial production of L-lactic acid from CCR and other biomass.

Effects of polysaccharides from abalone (Haliotis discus hannai Ino) on HepG2 cell proliferation.

Three polysaccharides, AAP, AVAP I, and AVAP II, were isolated from abalone Haliotis discus hannai Ino. The polysaccharides' compositions were analysed, and their effects on HepG2 cell proliferation were assessed. AVAP I had a greater growth-stimulatory effect than AAP or AVAP II. The oligosaccharide of AVAP I (Oli-AVAP I) exhibited the same growth effects, but rhamnose, the primary monosaccharide of AVAP I and Oli-AVAP I, did not exhibit this activity. Moreover, AVAP I dramatically reduced the mRNA levels of CDK6 and Cyclin E1 but significantly increased Cyclin B1, CDK1 and Cyclin F. Interestingly, AVAP I remained able to induce cell proliferation in a low serum concentration medium. AVAP I could therefore promote HepG2 cell proliferation by regulating gene expression and accelerating the cell cycle process. AVAP I may be useful as a serum supplement for stimulating the proliferation of mammalian cells. Our results offer a comprehensive method for utilising the abalone viscera, which is usually discarded as waste.

The protective effect of eicosapentaenoic acid-enriched phospholipids from sea cucumber Cucumaria frondosa on oxidative stress in PC12 cells and SAMP8 mice.

Alzheimer's disease (AD) is a common neurodegenerative disorders, in which oxidative stress plays an important role. The present study investigated the effect of eicosapentaenoic acid-enriched phospholipids (EPA-enriched PL) from the sea cucumber Cucumaria frondosa on oxidative injury in PC12 cells induced by hydrogen peroxide (H2O2) and tert-butylhydroperoxide (t-BHP). We also studied the effect of EPA-enriched PL on learning and memory functions in senescence-accelerated prone mouse strain 8 (SAMP8) in vivo. Pretreatment with EPA-enriched PL resulted in an enhancement of survival in a dose-dependent manner in H2O2 or t-BHP damaged PC12 cells. EPA-enriched PL pretreatment could also reduce the leakage of lactate dehydrogenase (LDH), and increase the intracellular total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity compared with the H2O2 or t-BHP group. The down-regulated Bcl-2 mRNA level and up-regulated Bax, Caspase-9, and Caspase-3 mRNA expression induced by H2O2 or t-BHP could be restored by EPA-enriched PL pretreatment. These results demonstrated that EPA-enriched PL exhibited its neuroprotective effects by virtue of its antioxidant activity, which might be achieved by inhibiting the mitochondria-dependent apoptotic pathway. The neuroprotective effect of EPA-enriched PL was also verified in vivo test: the EPA-enriched PL administration prevented the development of learning and memory impairments in SAMP8 mice. Our results indicated that EPA-enriched PL could offer an efficient and novel strategy to explore novel drugs or functional food for neuronprotection and cognitive improvement.

Improved inhibitory activities against tumor-cell migration and invasion by 15-benzylidene substitution derivatives of andrographolide.

In the present study, andrographolide (Andro, 1) derivatives were screened to identify potent inhibitors against tumor-cell migration and invasion, and associated structure-activity relationships were studied. Compared to 1, compounds 8a-8d exhibited more potent activities against migration in SGC-7901, PC-3, A549, HT-29 and Ec109 cell lines. Improved activities against tumor-cell migration and invasion were proved to be associated with the down-regulation of MMPs.

Protective effects of cerebrosides from sea cucumber and starfish on the oxidative damage in PC12 cells.

Neurodegenerative disorders are a class of diseases that have been linked to apoptosis induced by elevated levels of reactive oxygen species (ROS). The present study was undertaken to explore the effect of sea cucumber cerebrosides (SCC) and starfish cerebrosides (SFC) on the hydrogen peroxide (H2O2) and tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in PC12 cells. Cell viability, the leakage of lactate dehydrogenase (LDH), reactive oxygen species (ROS) level and superoxide dismutase (SOD) activity were determined for their effect on oxidative damage. Quantitative real-time PCR was investigated to analyze the mitochondrial genes expression. These results showed that both SCC and SFC decreased the leakage of LDH and intracellular ROS in a dose-dependent manner. SCC and SFC could also increase the SOD activity compared with the model groups. In H2O2 damage model, 400 µg/mL SCC increased the SOD activity by 79%, which was stronger than SFC. The results demonstrated that SCC and SFC exhibited the protective effects, which may be related to their antioxidant action. In addition, SCC and SFC dramatically increased the gene expression of B-cell lymphoma 2 (Bcl-2) but significantly decreased the gene expression of Cytochrome c, caspase9 and caspase3 compared with H2O2 or t-BHP treatment. These results suggested that SCC and SFC might exert a protective function against oxidative damage by inhibiting mitochondria-mediated apoptosis pathway. In conclusion, SCC and SFC played an important protective role in H2O2 and t-BHP-induced damage of PC12 cells, suggesting that the SCC and SFC may be a potential therapeutic agent against nervous system oxidative damage.

A novel evolutionarily conserved element is a general transcriptional repressor of p21WAF¹/CIP¹.

The effective induction of p21(WAF1/CIP1/Cdkn1a) (p21) expression in p53-negative cancer cells is an important avenue in cancer management. We investigated the ability of various common chemotherapeutic drugs to induce p21 expression in p53-negative cancer cells and showed that the induction of p21 expression by oxaliplatin is caused by the derepression of a previously unrecognized negative regulatory element with a Sp1/Sp3 palindrome sequence core at -216 to -236 of the p21 proximal promoter. Electrophoretic mobility shift and antibody super-shift assays confirmed the specific binding of Sp1/Sp3, and showed that the oxaliplatin-mediated derepression of p21 transcription was associated with an increased Sp1/Sp3 phosphorylation and binding affinity to the oxaliplatin-responsive element. A search of the ENCODE database for vertebrate-conserved genomic elements identified the Sp1/Sp3 palindrome element as the only vertebrate-conserved element within the 500-bp proximal p21 promoter region, indicating its fundamental importance. In in vivo competition assays, transfected synthetic Sp1/Sp3 palindrome elements derepressed the cotransfected or endogenous p21 promoter in a dosage-dependent manner. This derepression was not seen in oxaliplatin-treated cells, suggesting that the exogenous Sp1/Sp3 palindrome and oxaliplatin had the same downstream signaling target. Taken together, our results revealed, for the first time, this evolutionarily conserved Sp1/Sp3 palindrome element in the proximal p21 promoter that serves as a regulatory repressor to maintain p21 basal level expression.

[Protective effects of cerebroside from sea cucumber on the oxidative damage of PC12 cells induced by H2O2].

OBJECTIVE: To study the protective effects of cerebroside from sea cucumber (SCC) on the oxidative damage of PC12 cells induced by H2O2. METHODS: An oxidative damage model of PC12 cells was induced by H2O2. The survival rate of the cells was determined by MTT method. The leakage of LDH into cell cultures was determined to evaluate the degree of cell damage. The generation of intracellular reactive oxygen species (ROS) was detected by using DCFH-DA fluorescent probe. The activity of total antioxidation capacity (T-AOC) was determined by chemical colorimetric method and the SOD activity was measured by xanthine oxide method. RESULTS: The injury of PC12 cells induced by H2O2 could be reduced obviously by SCC. Compared with the model group, SCC could improve the survival rate of injured cells, reduce the leakage of LDH into cell culture and reduce intracellular ROS (P < 0.01), increase the intracellular T-AOC and SOD activity (P < 0.01). CONCLUSION: SCC has significantly protective effect on the injured PC12 cells induced by H2O2. The results would provide preliminary data on supporting the development of sea cucumber as a functional food, which might give benefits to our brain.