Estimation of lithium-ion battery health state using MHATTCN network with multi-health indicators inputs.

Accurately predicting the state of health (SOH) of lithium-ion batteries is fundamental in estimating their remaining lifespan. Various parameters such as voltage, current, and temperature significantly influence the battery's SOH. However, existing data-driven methods necessitate substantial data from the target domain for training, which hampers the assessment of lithium-ion battery health at the initial stage. To address these challenges, this paper introduces the multi-head attention-time convolution network (MHAT-TCN), amalgamating multi-head attention learning with random block dropout techniques. Additionally, it employs grey relational analysis (GRA) to select health indicators (HIs) highly correlated with battery capacity, thereby enhancing the accuracy of the model training. Employing leave-one-out crossvalidation (LOOCV), the MHAT-TCN network is pre-trained using data from batteries of the same model to facilitate comprehensive prediction of the target battery throughout its operational period. Results demonstrate that the MHAT-TCN network trained on HIs outperforms other models, enabling precise predictions across the entire operational period.

Liguzinediol potentiates the metabolic remodeling by activating the AMPK/SIRT3 pathway and represses Caspase-3/GSDME-mediated pyroptosis to ameliorate cardiotoxicity.

BACKGROUND: Liguzinediol (Lig) has emerged as a promising candidate for mitigating Doxorubicin (DOX)-induced cardiotoxicity, a significant limitation in the clinical application of this widely used antineoplastic drug known for its efficacy. This study aimed to explore the effects and potential mechanisms underlying Lig's protective role against DOX-induced cardiotoxicity. METHODS: C57BL/6 mice were treated with DOX. Cardiac function changes were observed by echocardiography. Cardiac structure changes were observed by HE and Masson staining. Immunofluorescence was applied to visualize the cardiomyocyte apoptosis. Western blotting was used to detect the expression levels of AMP-activated protein kinase (AMPK), sirtuin 3 (SIRT3), Caspase-3 and gasdermin E N-terminal fragment (GSDME-N). These experiments confirmed that Lig had an ameliorative effect on DOX-induced cardiotoxicity in mice. RESULTS: The results demonstrated that Lig effectively countered myocardial oxidative stress by modulating intracellular levels of reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD). Lig reduced levels of creatine kinase (CK) and lactate dehydrogenase (LDH), while ameliorating histopathological changes and improving electrocardiogram profiles in vivo. Furthermore, the study revealed that Lig activated the AMPK/SIRT3 pathway, thereby enhancing mitochondrial function and attenuating myocardial cell apoptosis. In experiments with H9C2 cells treated with DOX, co-administration of the AMPK inhibitor compound C (CC) led to a significant increase in intracellular ROS levels. Lig intervention reversed these effects, along with the downregulation of GSDME-N, interleukin-1ß (IL-1ß), and interleukin-6 (IL-6), suggesting a potential role of Lig in mitigating Caspase-3/GSDME-mediated pyroptosis. CONCLUSION: The findings of this study suggest that Lig effectively alleviates DOX-induced cardiotoxicity through the activation of the AMPK/SIRT3 pathway, thereby presenting itself as a natural product with therapeutic potential for preventing DOX-associated cardiotoxicity. This novel approach may pave the way for the development of alternative strategies in the clinical management of DOX-induced cardiac complications.

Bio-Inspired Superhydrophilic Self-Assembled Coronavirus-Like Pt-WC/CNT for Hydrogen Evolution Reaction.

This study presents a novel approach to enhance the catalytic activity of composite materials by promoting active surface exposure and improving hydrogen transfer performance. Through a self-assembly route involving tailored gas-solid and galvanic replacement reactions, Pt-WC/CNT catalysts with superhydrophilicity and coronavirus-like structure are synthesized. These unique structural features contribute to a remarkable enhancement in the electrocatalytic performance of the hydrogen evolution reaction (HER). Notably, the Pt-WC/CNT catalyst exhibits an outstanding intrinsic activity and efficient bubble transfer properties, leading to a high turnover frequency of 34.97 H2·s-1 at an overpotential of 100 mV. This value is 4.8 times higher than that achieved by commercial Pt/C catalysts (7.30 H2·s-1), establishing Pt-WC/CNT as one of the most active catalysts reported to date. Moreover, the combination of gas-solid and galvanic replacement reactions in the synthesis process offers a scalable route for the production of Pt-loading controllable composite catalysts, thus challenging the dominance of commercial Pt/C catalysts.

Modulating Dominant Facets of Pt through Multistep Selective Anchored on WC for Enhanced Hydrogen Evolution Catalysis.

Facilitating the exposure of the active crystal facets on the surfaces of composite catalysts is a representative route to promote catalytic activity. Based on a tailored galvanic replacement reaction, herein, a self-assembly route is reported to prepare Pt-WC/CNT with Pt (200) preferential orientation and well-dispersed structure, which are capable of substantially boosting electrocatalysis in hydrogen evolution reaction (HER). Formation mechanism reveals that the (200)-dominated Pt-based catalysts form in galvanic replacement reaction through selective anchored on WC, and the multistep galvanic replacement process plays a critical role to realize the Pt (200)-dominated growth in higher Pt loading catalyst. These unique structural features endow the Pt-WC/CNT with a high turnover frequency of 94.18 H2·s-1 at 100 mV overpotential, 7-fold higher than that of commercial Pt/C (13.55 H2·s-1), ranking it among the most active catalysts. In addition, this method, which combines with gas-solid reaction and galvanic replacement reaction, paves the way to scalable synthesis as Pt facets-controllable composite catalysts to challenge commercial Pt/C.

Inhibition of glutamine transporter ASCT2 mitigates bleomycin-induced pulmonary fibrosis in mice.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) represents a fatal pulmonary disease. Its mechanisms remain unclear and effective therapies are urgently needed. Glutaminolysis is involved in IPF pathology, but little is known about the role of ASCT2 responsible for cellular uptake of glutamine in IPF. We investigated the role of ASCT2 and its therapeutic implication in IPF through knockdown of ASCT2 in mice. METHODS: Mouse IPF model was established through a single intratracheal administration of bleomycin, and lentivirus-coated ASCT2 siRNA was administrated into mice via caudal vein for knockdown of ASCT2. Mouse blood and lung tissues were collected for biochemical, histological, and molecular examinations. RESULTS: ASCT2 siRNA significantly lowered ASCT2 expression in mouse lung tissues. Knockdown of ASCT2 reduced pulmonary levels of glutamic acid, α-ketoglutarate, glutathione and ATP, mitigated pulmonary histological injury, and reduced serum concentrations of pulmonary injury parameters including SP-A, SP-D, KL-6 and CCL18 in IPF mice. Moreover, serum levels of fibrotic parameters HA, LN, PC-III and IV-C were lowered by ASCT2 depletion. Collagen production and pulmonary hydroxyproline levels were also decreased by ASCT2 siRNA in IPF mice, which was concomitant with downregulation of α-smooth muscle actin, collagen type Iα1 and transforming growth factor-ß receptor II. Furthermore, ASCT2 deficiency downregulated the mRNA and protein expression of inflammatory cytokines IL-1ß and TNF-α as well as macrophage marker F4/80 in lung tissues of IPF mice. CONCLUSIONS: Inhibition of ASCT2 effectively mitigated pulmonary injury, fibrosis and inflammation in mice with bleomycin-induced IPF. ASCT2 could be a novel therapeutic target for treatment of IPF.

Highly dispersed silver imbedded into TiN submicrospheres for electrochemical detecting of hydrogen peroxide.

We report the fabrication of silver nanoparticles evenly imbedded into TiN submicrospheres via one-pot solvothermal reaction and subsequent nitridation for electrochemical detecting of hydrogen peroxide. The precursor of TiO2 submicrospheres and high dispersion of silver nanoparticles are regulated by the alcoholysis of tetrabutyl titanate and reducibility of enol in vitamin C. The ion nitriding promoted the conductivity and micro-nano porous structure on the surface of TiN submicrospheres, which increase the dispersity of silver nanoparticles and make contributions to avoid aggregations. More importantly, the electrochemical response of Ag-TiN submicrospheres to H2O2 was remarkably enhanced due to the co-effects of Ag and N-doping. It provides a superior sensing performance for electrochemical detection of hydrogen peroxide at - 0.3 V with a high sensitivity of 33.25 µA mmol L-1 cm-2, wide linear range of 0.05-2100 µM and low detection limit of 7.7 nM. The fabricated sensor also reliably applied in detection of H2O2 in milk samples with good reproducibility, repeatability and storage stability.

The public health response to the COVID-19 outbreak in mainland China: a narrative review.

The COVID-19 pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused nations to adopt unprecedented control measures in order to curb its spread. As the first nation to respond, China's aggressive control measures appeared to have been effective in suppressing the first wave and keeping new cases under control. Here, we provide the historical context and details of China's public health response to COVID-19. We highlight the lessons and impact of the 2002-2003 SARS outbreak, which demonstrated the importance of transparency, surveillance and testing laboratories during an outbreak. We provide an overview of China's response strategy that was based on the principles of early detection, isolation, management and treatment and involved not only the large-scale coordination of multiple governmental bodies but also grass-root community participation throughout the country. These community-based organizations conducted active surveillance for febrile cases and provided support for those in quarantine and communities in lockdown. Importantly, these broader measures were supported by digital technology, including the extensive use of internet-based platforms and mobile applications (APPs). While there have been no significant increases in case numbers since April, there is still much concern over a second wave, considering the resumption of work and school, the lifting of travel restrictions and the outbreaks occurring globally. Control measures has since been implemented by provincial authorities, which includes continued surveillance and rapid testing. Although China's strict control measures may not suit every nation, the principles of early detection and isolation continue to hold true and have been a cornerstone of the initial and ongoing response to the COVID-19.

Puerarin promotes the viability and differentiation of MC3T3-E1 cells by enhancing LC3B-mediated autophagy through downregulation of miR-204.

Puerarin is a bioactive substance extracted from Pueraria lobata. It is known to promote the viability, differentiation and mineralization of osteoblasts. However, the molecular mechanisms involved in these activities are not well understood. The present study was conducted with the aim of elucidating the effect of puerarin on osteoblasts and to explore the underlying mechanism. CCK-8 analysis showed that puerarin (0.1, 1 and 10 µM) promoted the viability of osteoblastic MC3T3-E1 cells, with 1 µM of puerarin exhibiting the strongest effect. Moreover, 1 µM puerarin significantly increased the activity of alkaline phosphatase (ALP) and the formation of mineralized nodules in the MC3T3-E1 cells. Treatment with 1 µM puerarin for 72 h led to a significant upregulation in the expression level of microtubule-associated light chain 3 (LC3)B and Beclin1 proteins. This treatment was more effective in promoting LC3B expression than what was observed following treatment with rapamycin (overexpression for autophagy). The bilayer membrane structure of autophagosomes was observed by electron microscopy. Conversely, 3-methyladenine (3-MA, inhibitor of autophagy) reduced the cell viability as well as the activity of alkaline phosphatase (ALP) in MC3T3-E1 cells, although, there was no significant influence on mineralization. Prediction results of the biological information showed that LC3B could be a direct target of microRNA-204 (miR-204). In the present study, the expression level of miR-204 was decreased by puerarin. miR-204 mimics significantly decreased LC3B expression and inhibited auotophagosome formation, while the miR-204 inhibitor had the opposite effects. To conclude, the results of the present study suggest that puerarin promotes the viability and differentiation of MC3T3-E1 cells through autophagy, which is possibly associated with miR-204-regulated LC3B upregulation.

Puerarin inhibits TRPM3/miR-204 to promote MC3T3-E1 cells proliferation, differentiation and mineralization.

Puerarin is an isoflavonoid phytoestrogen extracted from the root of Radix Pueraria, has attracted increasing attention because of its beneficial effects on anti-osteoporosis, but the molecular mechanisms underlying its actions on osteoblasts are not fully understood. The current study aimed to investigate the effect of puerarin on MC3T3-E1 osteoblastic cells proliferation, differentiation and mineralization, in vitro and its underlying mechanisms. The results indicated that puerarin significantly promoted the osteoblasts proliferation, enhanced alkaline phosphatase activity and increased the formation of mineralized nodules. Following treatment with puerarin, the expression levels of transient receptor potential Melastatin 3 (TRPM3) and microRNA-204 (miR-204) were decreased, whereas that of Runt-related transcription Factor 2 (Runx2) increased. TRPM3-small interfering RNA and 2-aminoethoxydiphenyl borate (2-APB, inhibitor of TRPM3) promoted the expression of Runx2 and thus improved the development of osteoblasts, but pregnenolone sulfate, which is the agonist of TRPM3, inhibited the effects. In addition, puerarin induced the changes of intracellular Ca2+ concentration ([Ca2+ ]i ) and extracellular Ca2+ concentration ([Ca2+ ]0 ) through TRPM3 might be involved in the biological process of MC3T3-E1 cells. These results suggested that puerarin may promote MC3T3-E1 cell proliferation, differentiation and mineralization, which may be related to the downregulation of TRPM3/miR-204 and following regulating [Ca2+ ]i and [Ca2+ ]0 , and activation of Runx2.

Puerarin promotes the viability and differentiation of MC3T3­E1 cells by miR­204­regulated Runx2 upregulation.

Puerarin has attracted increasing attention because of its beneficial effects on anti­osteoporosis, but the molecular mechanisms underlying its actions on osteoblasts are not fully understood. The current study aimed to investigate the effect of puerarin on the cell viability and differentiation of mouse MC3T3­E1 osteoblast­like cells in vitro and its underlying mechanisms. The results indicated that 0.01, 0.1 and 1 mg/ml puerarin significantly promoted the viability of osteoblasts, enhanced alkaline phosphatase (ALP) activity and increased the expression of transforming growth factor­ß1, Smad2, Smad3 and Runt­related transcription factor (Runx)2. Micro (mi)RNA target prediction programs predicted that miR­204 may directly target Runx2. Following treatment with 0.1 mg/ml puerarin for 48 h, the expression level of miR­204 was downregulated. Besides, miR­204 dramatically repressed the luciferase activity of wildtype Runx2 3'­UTR transfected cells, but not that of the mutant ones. Overexpression of miR­204 in osteoblasts significantly decreased the protein expression of Runx2, while inhibition of miR­204 enhanced Runx2's expression. In addition, overexpression of miR­204 inhibited the cell viability and ALP activity of osteoblasts, while inhibition of miR­204 had the opposite effect. The results suggested that puerarin may promote MC3T3­E1 osteoblast­like cell viability and differentiation, which may be related to the downregulation of miR­204 and the following activation of Runx2.

Platycodin-D Induced Autophagy in Non-Small Cell Lung Cancer Cells via PI3K/Akt/mTOR and MAPK Signaling Pathways.

Platycodin-D (PD) is an effective triterpene saponin extracted from the root of Platycodon grandiflorum which has been used clinically to treat pulmonary diseases in traditional Chinese medicine. Recently, it has been reported that PD has anti-tumor effects in various cancer models through the induction of apoptosis. However, whether PD induces autophagy in both cell lines and its molecular mechanisms have not been elucidated. Here, our present study confirmed that PD induced autophagy in both NCI-H460 and A549 cells via up-regulating the expression levels of Atg-3, Atg-7 and Beclin-1. Meanwhile, PD contributed to the up-regulation of LC3-II at both protein and mRNA levels. Further detection of the PI3K/Akt/mTOR signaling pathway compared to LY294002 (PI3K kinase inhibitor), RAP (mTOR kinase inhibitor) and insulin (an activator of PI3K/Akt/mTOR signaling pathway) showed that PD induced autophagy through inhibiting the pathway at p-Akt (Ser473), p-p70S6K (Thr389) and p-4EBP1 (Thr37/46) in both cell lines. Moreover, the examination of MAPK signaling pathway showed that PD treatment increased the phosphorylation of JNK and p38 MAPK, while decreased the phosphorylation of Erk1/2 in both cell lines. Additionally, the effects assessed with a panel of pharmacologic inhibitors, including U0126 (Erk1/2 kinase inhibitor), SP600125 (JNK kinase inhibitor) and SB203580 (p38 MAPK kinase inhibitor) suggested that the activation of JNK and p38 MAPK participated in PD-induced autophagy. Taken together, these findings suggested that PD induced autophagy in NCI-H460 and A549 cells through inhibiting PI3K/Akt/mTOR signaling pathway and activating JNK and p38 MAPK signaling pathways. Therefore, PD may be an alternative compound for NSCLC therapy.

Daucosterol protects neurons against oxygen-glucose deprivation/reperfusion-mediated injury by activating IGF1 signaling pathway.

We previously reported that daucosterol (a sterolin) up-regulates the expression of insulin-like growth factor I (IGF1)(1) protein in neural stem cells. In this study, we investigated the effects of daucosterol on the survival of cultured cortical neurons after neurons were subjected to oxygen and glucose deprivation and simulated reperfusion (OGD/R)(2), and determined the corresponding molecular mechanism. The results showed that post-treatment of daucosterol significantly reduced neuronal loss, as well as apoptotic rate and caspase-3 activity, displaying the neuroprotective activity. We also found that daucosterol increased the expression level of IGF1 protein, diminished the down-regulation of p-AKT(3) and p-GSK-3ß(4), thus activating the AKT(5) signal pathway. Additionally, it diminished the down-regulation of the anti-apoptotic proteins Mcl-1(6) and Bcl-2(7), and decreased the expression level of the pro-apoptotic protein Bax(8), thus raising the ratio of Bcl-2/Bax. The neuroprotective effect of daucosterol was inhibited in the presence of picropodophyllin (PPP)(9), the inhibitor of insulin-like growth factor I receptors (IGF1R)(10). Our study provided information about daucosterol as an efficient and inexpensive neuroprotectants, to which the IGF1-like activity of daucosterol contributes. Daucosterol could be potentially developed as a medicine for ischemic stroke treatment.

Discrepancy between the effects of morronside on apoptosis in human embryonic lung fibroblast cells and lung cancer A549 cells.

Morroniside is a water-soluble compound extracted from the fruit of Cornus officinalis and is used to protect lung activity against aging. In the present study, the manner in which morroniside regulates normal lung and cancer cells was examined. The human embryonic lung fibroblast (HELF) cell line and lung cancer A549 cell line, and their responses to morroniside treatment, were examined. Results showed that morroniside reverses the apoptotic effect of H2O2 on HELF cell growth, protecting cell proliferation and normal cell morphology and inhibiting apoptosis. However, these effects were not present in A549 cells. Western blotting showed that morroniside also markedly downregulated retinoblastoma protein in HELF cells. These results suggest that morroniside treatment exhibits different effects on apoptosis in HELF and A549 cells, making it a viable compound for decreasing the side effects of anticancer medicines in normal cells.

Daucosterol promotes the proliferation of neural stem cells.

Neural stem cells (NSCs) are self-regenerating cells, but their regenerative capacity is limited. The present study was conducted to investigate the effect of daucosterol (a sterolin) on the promotion of NSC proliferation and determine the corresponding molecular mechanism. Results of cell counting kit-8 (CCK-8) assay showed that daucosterol significantly increased the quantity of viable cells and the effectiveness of daucosterol was similar to that of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF). Flow cytometry detection of CFSE-labeled (CFSE, carboxyfluorescein diacetate succinimidyl ester) NSCs showed that Div Index (or the average number of cell divisions) and % Divided (or the percentage of cells that divided at least once) of the cells were increased, indicating that daucosterol increased the percentage of NSCs re-entering the cell cycle. mRNA microarray analysis showed that 333 genes that are mostly involved in the mitotic cell cycle were up-regulated. By contrast, 627 genes that are mostly involved in differentiation were down-regulated. In particular, insulin-like growth factor I (IGF1) was considered as an important regulatory gene that functionally promoted NSC proliferation, and the increased expression of IGF1 protein was validated by ELISA. In addition, the phosphorylation of AKT was increased, indicating that the proliferation-enhancing activity of daucosterol may be involved in IGF1-AKT pathway. Our study provided information about daucosterol as an efficient and inexpensive growth factor alternative that could be used in clinical medicine and research applications.

[Study on synergistic effect of sodium cantharidinate combined with chemotherapeutic drugs on hepatic carcinoma and its effective mechanism].

OBJECTIVE: To study the synergistic effect on hepatoma cell(SMMC-7721) and the reduction killing effect on normal liver cells(LO-2) treated with sodium cantharidinate (SCA) in combination with fluorouracil(5-FU) or cisplatin(DDP) as well as the related mechanism. METHODS: MTT assay was used to select the best ratio of SCA with 5-FU or SCA with DDP which had less toxicity on LO-2 cell line and had synergistic effect on SMMC-7721 cell line; Flow cytometry assay was used to analyze the apoptosis-induction of the different ratio of drugs on both cell lines; Hoechst-33258 fluorescent staining assay was used to observe the nuclear morphological changes of cells; Immunoblotting assay was used to analyze the Ras/Raf/ERK1/2 signaling pathway and the apoptosis related signaling pathway in both cell lines. RESULTS: MTI assay indicated that the proliferation inhibition of SCA,5-FU and DDP on SMMC-7721 cell line was in a time-and dose-dependent manner respectively. Among them, SCA had a more significant inhibition on SMMC-7721 cell line than on LO-2 after 12 h or 24 h treatment (P <0. 01). Moreover, after a treatment of 48 h,the ratio of 2. 5 µg/mL SCA and 2 µg/mL DDP showed a more significant inhibition on SMMC-7721 cell line than on LO-2 cell line,which was then be considered as the optimal concentration ratio for the following experiment. Co-treatment of SCA (2. 5 µg/mL) with DDP (2 µg/mL) induced a more significant apoptosis on SMMC-7721 cell line compared with single treatment with SCA (2. 5 µg/mL) or DDP (2 µg/mL) respectively (P < 0. 01). After a 48 h treatment of the optimal ratio of drugs, the significant morphological apoptotic characteristics were observed both under inverted microscope and by Hoechst-33258 fluorescent staining assay in both cell lines. The results of Western blot assay showed that this ratio of drugs could significantly increase the protein expression of Bax,P53 and P21 and decreased the expression of BCL-2, Casepase-3, p-Erk, p-Ras and p-c-Raf in SMMC-7721 cells. Meanwhile,the effect on the proteins mentioned above was lesser in LO-2 cells. CONCLUSION: These results indicates that 2. 5 µg/mL SCA + 2 µg/mL DDP showed a higher inhibition on the hepatic carcinoma cells and a relatively lower cytotoxicity on normal liver cells. The major anti-cancer mechanism is related with the inhibition on Erk signaling pathway and the induction of apoptosis through the mitochondrial pathway.

Microarray Analysis of mRNA and MicroRNA Expression Profile Reveals the Role of ß -Sitosterol-D-glucoside in the Proliferation of Neural Stem Cell.

Neural stem cells (NSCs) are self-regenerating cells, but their regenerative capacity is limited. The present study was conducted to investigate the effect of ß -sitosterol-D-glucoside (BSSG) on the proliferation of hippocampal NSCs and to determine the corresponding molecular mechanism. Results of CCK-8 assay showed that BSSG significantly increased NSC proliferation and the effectiveness of BSSG was similar to that of basic fibroblast growth factor and epidermal growth factor. mRNA expression profiling showed that 960 genes were differentially expressed after NSCs were treated with BSSG. Among the 960 genes, IGF1 is considered as a key regulatory gene that functionally promotes NSC proliferation. MicroRNA (miRNA) expression profiling indicated that 30 and 84 miRNAs were upregulated and downregulated, respectively. miRNA-mRNA relevance analysis revealed that numerous mRNAs including IGF1 mRNA were negatively regulated by miRNAs with decreased expression, thereby increasing the corresponding mRNA expression. The increased expression of IGF1 protein was validated by ELISA. Picropodophyllin (PPP, an inhibitor of IGF-1R) inhibition test confirmed that the proliferation-enhancing effect depended on IGF1. This study provided information about BSSG as an efficient and inexpensive growth factor alternative, of which the effect is closely involved in IGF1.

5-Hydroxymethylfurfural from wine-processed Fructus corni inhibits hippocampal neuron apoptosis.

Previous studies have shown that 5-hydroxymethylfurfural, a compound extracted from wine-processed Fructus corni, has a protective effect on hippocampal neurons. The present study was designed to explore the related mechanisms. Our study revealed that high and medium doses (10, 1 µmol/L) of 5-hydroxymethylfurfural could improve the morphology of H2O2-treated rat hippocampal neurons as revealed by inverted phase-contrast microscopy and transmission electron microscopy. MTT results showed that incubation with high and medium doses of 5-hydroxymethylfurfural caused a significant increase in the viability of neuronal cells injured by H2O2. Flow cytometry assays firmed that H2O2 could induce cell apoptosis, while high and medium doses of 5-hydroxymethylfurfural had a visible protective effect on apoptotic rat hippocampal neurons. Real-time PCR and western blot analysis showed that high and medium doses of 5-hydroxymethylfurfural prevented H2O2-induced up-regulation of p53, Bax and caspase-3 and an-tagonized the down-regulation of Bcl-2 induced by H2O2 treatment. These results suggested that 5-hydroxymethylfurfural could inhibit apoptosis of cultured rat hippocampal neurons injured by H2O2 via increase in Bcl-2 levels and decrease in p53, Bax and caspase-3 protein expression levels.

[Effect of 5-hydroxymethyl furfural on BCL-2 and NF-kappaB gene expression of apoptotic rat hippocampal neurons injured by H2O2].

OBJECTIVE: To investigate the effect of 5-hydroxymethyl furfural (5-HMF) on apoptosis and BCL-2, NF-kappaB gene expression of rat hippocampal neurons injured by hydroperoxide (H2O2). METHODS: Hippocampal neurons of newly born rat were cultured in vivo and injured by H2O2. Effect of different concentration of 5-HMF on cell viability was measured by MTT. Flow cytometer (FCM) was used to measure the apoptosis of rat hippocampal neurons pre-cultured with different concentration of 5-HMF,Western blotting was used to measure the expression of BCL-2 and NF-kappaB gene. RESULTS: It revealed that the high and medium dosage of 5-HMF could increase the activity of rat hippocampal. The high, medium and low dosage of 5-HMF also increased the expression of BCL-2 gene and decreased the expression of NF-kappaB gene. CONCLUSION: 5-HMF could restrain the apoptosis of cultured hippocampal neurons injured by H2O2. The mechanism may be related to increasing in BCL-2 level and decreasing in NF-kappaB level.

Investigation on the morphological protective effect of 5-hydroxymethylfurfural extracted from wine-processed Fructus corni on human L02 hepatocytes.

AIM: To determine the mode of action of 5-hydroxymethylfurfural (5-HMF) extracted from wine-processed Fructus corni on hepatoprotective activities, the effects of 5-HMF on H(2)O(2)-induced human L02 hepatocytes injury was examined. MTHODS: Hepatocytes L02 injured by H(2)O(2) was treated by 5-HMF. The morphological changes of the cells were observed under inverted phase-contrast, fluorescence, and transmission electron microscopy and the activities of caspase-9 and caspase-3 were tested by enzyme-linked immunosorbent detector. RESULTS: It revealed that 5-HMF improved the morphology of H(2)O(2)-treated human L02 hepatocytes, and also inhibited the level of caspase-9 and caspase-3 of them. CONCLUSIONS: These results suggested a morphological hepatocyte protective effect and the anti-apoptosis mechanism by 5-HMF.

2',4'-Dihydroxychalcone-induced apoptosis of human gastric cancer MGC-803 cells via down-regulation of survivin mRNA.

2',4'-Dihydroxychalcone (TFC), a main component in Herba Oxytropis, is grouped under flavonoids, which are well known to have antitumor activities in vitro. In this study, the possible antitumor mechanism of TFC in human gastric cancer MGC-803 cells is examined. Hoechst 33258 staining analysis indicates that TFC causes MGC-803 cell shrinkage and apoptotic body formation, typical characteristics of apoptosis. Flow cytometric analysis demonstrates that TFC causes cell cycle arrest in the G2/M phase. Furthermore, TFC significantly increases caspase-3 activity but decreases survivin mRNA expression. Therefore, TFC can induce the apoptosis of MGC-803 cells via down-regulation of survivin mRNA expression.