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《园艺学报》是中国园艺学会和中国农业科学院蔬菜花卉研究所主办的学术期刊,创刊于1962年,刊载有关果树、蔬菜、观赏植物、茶及药用植物等方面的学术论文、研究报告、专题文献综述、问题与讨论、新技术新品种以及园艺研究动态与信息等,适合园艺科研人员、大专院校师生及农业技术推广部门专业技术人员阅读参考。《园艺学报》是中文核心期刊,被英国《CAB文摘数据库》、美国CA化学文摘、日本CBST科学技术文献速     

Panax quinquefolium saponins protect rat myocardium from ischemia/reperfusion injury through attenuating excessive endoplasmic reticulum stress

AIM: To investigate whether excessive endoplasmic reticulum stress (ERS) is involved in the protective mechanism of Panax quinquefolium saponins (PQS) against ischemia/reperfusion (I/R) injury in rat myocardium. METHODS: The model of myocardial I/R injury in vivo was made by ligating the left anterior descending artery for 45 min followed by 24 h of reperfusion in SD rats. The hemodynamics and serum content of cardiac troponin T (cTnT) were measured. The myocardial infarct size was measured by Evans blue and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. Cardiomyocyte apoptosis was detected using in situ TDT-mediated dUTP nick end labeling (TUNEL). The protein levels of glucose-regulated protein 78 (GRP78), calreticulin (CRT), C/EBP homologous protein (CHOP), caspase-12, apoptosis-associated proteins Bax and Bcl-2 were determined by Western blotting. RESULTS: Compared with I/R group, the mean arterial pressure in PQR+IR group was decreased by 32.0%, and left ventricular±dp/dtmax was increased by 64.0% and 35.0%, respectively.The serum content of cTnT was decreased by 53.3%, the percentage of area of necrosis (AN)/area at risk (AAR) was reduced by 65.5% and the apoptosis rate was decreased by 54.9%.The myocardial pathological changes were improved. Bcl-2 protein expression was increased by 110.0% and that of Bax was decreased by 47.8%. CRT protein expression was decreased by 43.4 %, CHOP protein expression and the protein level of cleaved caspase-12 were decreased by 38.6% and 23.7% in PQS+I/R group. CONCLUSION: PQS alleviates I/R injury in myocardium by inhibition of excessive ERS.     

Effects of T-cadherin on hypoxia/reoxygenation-induced apoptosis of cardiomyocytes from neonatal rats

AIM: To investigate the mechanism of cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) by silencing a new adiponectin receptor T-cadherin through adenovirus-mediated RNA interference. METHODS: The primary cardiomyocytes were isolated from neonatal rats and cultured for 72 h. The cardiomyocytes were randomly divided into control group, H/R group, APN+H/R group, Ad-T-cadherin-siRNA+APN+H/R group and Ad-HK (adenovirus negative control)+APN+H/R group. The transfection ability and efficiency were examined. The expression of T-cadherin at mRNA and protein levels was detected by RT-PCR and Western blotting. The apoptotic rate was analyzed by flow cytometry and TUNEL. RESULTS: High purity of neonatal rat cardiomyocytes was obtained by primary culture. After 48 h, over 90% of myocardiocytes were infected at MOI=100. The transfected myocardiocytes showed a low expression level of T-cadherin under normal physiological condition. Compared with APN+H/R group, the cell apoptotic rate significantly increased in Ad-T-cadherin-siRNA+APN+H/R group (P<0.05). Compared with H/R group, the difference was not statistically significant (P>0.05). CONCLUSION: Ad-T-cadherin-siRNA effectively infects myocardial cells in vitro and successfully reduces the expression of T-cadherin in myocardial cells. The inhibitory effect of adiponectin on H/R-induced cardiomyocyte apoptosis is attenuated by decreasing the expression of T-cadherin.     

Effects of PDCD5 on hypoxia/reoxygenation-induced autophagy and apoptosis of cardiomyocytes

AIM: To investigate the influence of programmed cell death 5 (PDCD5) on apoptosis and autophagy in the cardiomyocytes exposed to hypoxia/reoxygenation (H/R) and its potential mechanism.METHODS: H9c2 cells were exposed to H/R. PDCD5 was downregulated by RNA interference. The cell viability was measured by MTT assay. TUNEL assay was used to detect cell apoptosis. The mRNA and protein levels were determined by RT-qPCR and Western blot.RESULTS: The expression of PDCD5 was upregulated in the cardiomyocytes after H/R injury. Furthermore, H/R injury obviously reduced the cell viability and enhanced the apoptosis and autophagy of the cardiomyocytes. However, knockdown of PDCD5 increased the cell viability, and attenuated H/R-induced apoptosis, accompany with reduction of Bax and augment of Bcl-2 expression. Additionally, silencing PDCD5 markedly inhibited H/R-induced autophagy by regulating the expression of LC3-II/LC3-I and beclin-1. Moreover, downregulation of PDCD5 suppressed NF-κB signaling by redu-cing the protein level of p-P65.CONCLUSION: Silencing PDCD5 suppresses H/R-induced H9c2 cells apoptosis and autophagy by blocking NF-κB signaling pathway. The result indicates a new strategy for the prevention and treatment of myocardial I/R injury.     

Panax notoginseng saponins suppress oxygen-glucose deprivation/reoxygenation-induced pyroptosis of SH-SY5Y cells

AIM To investigate the effect of Panax notoginseng saponins (PNS) on pyroptosis of SH-SY5Y cells induced by oxygen-glucose deprivation/reoxygenation (OGD/R). METHODS The OGD/R was conducted to induce ischemia/reperfusion injury in SH-SY5Y cells. The effects of PNS on the viability (detected by CCK-8 assay) and membrane permeability [indicated by lactate dehydrogenase (LDH) leakage and propidium iodide (PI) staining positive cell proportion] of OGD/R-induced SH-SY5Y cells were observed. The protein levels of gasdermin D (GSDMD), GSDMD N-terminal fragment (GSDMD-N), caspase-1 and caspase-4, and the release of interleukin-1β (IL-1β) and IL-18 in the cells were also determined. RESULTS After exposure to OGD/R, the viability of SH-SY5Y cells dramatically decreased (P<0.01), while the LDH leakage, the PI staining positive cell proportion, the protein levels of GSDMD, GSDMD-N, caspase-1 and caspase-4, and the release of IL-1β and IL-18 were significantly increased (P<0.01). However, PNS treatment enhanced the viability of SH-SY5Y cells inhibited by OGD/R (P<0.01), but reduced the leakage of LDH and the percentage of PI staining positive cells (P<0.05 or P<0.01). Moreover, PNS reversed the increases in the protein levels of GSDMD, GSDMD-N, caspase-1 and caspase-4 and the release of IL-1β and IL-18 in OGD/R-induced SH-SY5Y cells (P<0.05 or P<0.01). CONCLUSION Treatment with PNS alleviates OGD/R-induced injury in SH-SY5Y cells. Its mechanism may be related to inhibition of SH-SY5Y cell pyroptosis induced by OGD/R.     

Protective effect of morinda officinalis oligosaccharides monomer HexB on hypoxia/reoxygenation-induced injury in HUVECs

AIM:To explore the protective effect of morinda officinalis oligosaccharides monomer HexB on hypoxia/reoxygenation (H/R)-induced injury in human umbilical vein endothelia cells (HUVECs). METHODS:HUVECs were treated with HexB, 4-phenylbutyric acid (4-PBA) and thapsigargin (TG), respectively. The cells were divided into control group, HexB group, H/R group, HexB+H/R group, 4-PBA+H/R group, TG group and HexB+TG group. The cell viability was measured by CCK-8 assay. The apoptotic rate was detected by flow cytometry. Western blot was used to determine the protein levels of endoplasmic reticulum stress (ERS) related molecules chaperone protein glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), apoptosis-related protein caspase-12 and phosphorylated c-Jun NH₂-terminal kinase (p-JNK). RESULTS:The viability of HUVECs was reduced in H/R group and TG group (P<0.05), increased in HexB+H/R, 4-PBA+H/R and HexB+TG group (P<0.05). The apoptotic rate, the protein levels of GRP78, CHOP, caspase-12 and p-JNK were increased in H/R group and TG group (P<0.05), weakened in the HexB+H/R group (P<0.05), 4-PBA+H/R group and HexB+TG group (P<0.05). No significant change in the apoptotic rate, cell viability, protein levels of GRP78, CHOP, caspase-12, p-JNK between HexB+H/R group and 4-PBA+H/R group was observed. CONCLUSION:HexB attenuates HUVECs injury caused by H/R through suppressing ERS and apoptosis. The possible mechanism may be involved in the apoptotic pathways related to GRP78, CHOP, caspase-12 and p-JNK.     

Effects of Panax quinquefolium saponin on mitochondrial membrane potential and cardiomyocyte apoptosis in ischemia/reperfusion rats

AIM：To investigate whether mitochondrial membrane potential (ΔΨm) and the mitochondrial apoptotic pathway are involved in the protective mechanism of Panax quinquefolium saponin (PQS) against cardiomyocyte apoptosis after ischemia/reperfusion (I/R) injury in rat myocardium. METHODS：Ninety healthy male SD rats were randomly divided into sham group, I/R group, PQS (200 mg·kg-1·d-1) +I/R group, cyclosporine A (CsA) group, CsA (10 mg·kg-1) +I/R group and PQS +CsA +I/R group. The model of myocardial I/R injury in vivo was established by ligating the left anterior descending artery (LAD) for 30 min followed by 120 min of reperfusion in the rats. The serum activity of lactate dehydrogenase (LDH) was measured by automatic chemistry analyzer. The myocardial infarct size was measured by Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. Cardiomyocyte apoptosis was detected by in situ TDT-mediated dUTP nick end labeling (TUNEL). The protein levels of Bcl-2, Bax, cleaved caspase-3 and cytosolic cytochrome C were determined by Western blotting. ΔΨm was measured by laser scanning confocal microscopy and fluorescence microplate reader. RESULTS：Compared with I/R group, the serum content of LDH,the infarction size in PQS+I/R group, CsA+I/R group and PQS+CsA+I/R group and the myocardial apoptotic index were decreased. Compared with I/R group, the fluorescence intensity of mitochondria after JC-1 staining was enhanced in PQS+I/R group, CsA+I/R group and PQS+CsA+I/R group, and the relative fluorescence units (RFU) of ΔΨm were improved in those 3 groups. In PQS+I/R group, CsA+I/R group and PQS+CsA+I/R group, the protein expression of Bcl-2 was increased, and that of Bax was decreased compared with I/R group. Moreover, in those 3 groups, the protein levels of cleaved-caspase-3 and cytosolic cytochrome C were decreased compared to I/R group, respectively. CONCLUSION：PQS attenuates myocardial injury and cardiomyocyte apoptosis during I/R, and the protective mechanisms of PQS were associated with the modulation of ΔΨm and the inhibition of mitochondrial apoptosis pathway.     

Anti-aging Klotho protein reduce the hypoxia/reoxygenation injury of neonatal rat myocardial cells

AIM: To study the effects of anti-aging Klotho protein on neonatal rat myocardial cells with hypo-xia/reoxygenation (H/R) injury. METHODS: The cardiomyocytes of neonatal SD rats were cultured to establish hypoxia/reoxygenation model. The myocardial cells were divided into normal control group, H/R model group, different concentrations of Klotho protein (0.1 μmol/L, 1 μmol/L and 10 μmol/L) pretreatment groups. The myocardial cells pulse frequency was observed before and after H/R. The cell viability was measured by MTT assay. The leakages of LDH, CK and AST, the content of MDA and the activity of SOD were detected. The apoptotic rate of the myocardial cells was analyzed by flow cytometry. The mRNA expression of endoplasmic reticulum stress markers and apoptosis-related molecules GRP78, CRT, CHOP and caspase-12 was measured by real-time PCR. The protein levels of CHOP, caspase-12 and phosphorylated Akt in the myocardial cells were determined by Western blot. RESULTS: Compared with normal control group, the pulse frequency, cell viability rate and SOD activity of myocardial cells were significantly decreased, the cell apoptotic rate as well as the contents of LDH, CK, AST and MDA were increased in H/R model group. The mRNA expressions of GRP78, CRT, CHOP and caspase-12 as well as the protein levels of CHOP and caspase-12 were increased, whereas p-Akt level was decreased obviously. Compared with H/R model group, the pulse frequency, cell viability rate and SOD activity were increased significantly, the cell apoptotic rate as well as the contents of LDH, CK, AST and MDA were decreased in Klotho pretreated group. The mRNA expression of GRP78, CRT, CHOP and caspase-12 as well as the protein levels of CHOP and caspase-12 were decreased, while p-Akt level increased significantly. CONCLUSION: Anti-aging Klotho protein improves the myocardial cell survival and inhibits the apoptosis by increasing the resistance of the cells to oxidative stress and excessive endoplasmic reticulum stress response, which is related with the activation of Akt phosphorylation in H/R-injured mycardial cells.     

西洋参发根器官发生及再生植株研究

以西洋参播种苗切断儿为外植体,由发根农杆菌R1601诱导发状根,通过器官发生途径建立高频再生体系,建立西洋参悟性快速繁殖体系。结果表明:诱导西洋参发根脱分化成愈伤组织的最佳培养基为:MS+2,4-D 2.0mg/L+KT 0.5mg/L诱导不定芽增殖和分化的培养基为MS+KT 0.2mg/L+IBA 0.5mg/L诱导生根的培养基为1/2MS+GA₃ 5.0mg/L+IBA0.5mg/L+NAA 2.0mg/L。     

2,4-D对成熟与非成熟西洋参种胚体细胞胚发生的影响

以西洋参成熟种子及未成熟种子为试材,在无菌操作条件下剥取种胚,将其依次接种在不同2,4-D浓度的MS培养基中,在光照和暗培养条件下分别进行培养,研究2,4-D对西洋参种胚体细胞胚发生的影响.结果表明:成熟种胚在不同浓度2,4-D中皆可发生体细胞胚,最佳浓度为0.5 mg/L,光照可以促进体细胞胚发生;未成熟种胚不能形成体细胞胚.说明成熟种胚体细胞胚发生需要2,4-D诱导,未成熟种胚的表现与成熟种胚差异显著;西洋参种胚在发育控制上与人参存在明显不同.     

Role of ROS/PKC/p38 MAPK pathway in protective effects of polysaccharide from Fructus cornion rat cardiomyocytes against hypoxia-reoxygenation injury

AIM: To investigate the effect of polysaccharide from Fructus corni(PFC) on cardiomyocytes against hypoxia/reoxygenation (H/R) injury and its possible relationship with ROS/PKC/p38 MAPK pathway.METHODS: Primary cardiomyocytes were isolated from neonatal SD rats and randomly divided into normal group, H/R group, PFC (20 mg/L, 100 mg/L and 200 mg/L) preconditioning+H/R groups, chelerythrine+PFC (100 mg/L)+H/R group and SB203580+PFC (100 mg/L)+H/R group. The cell viability was measured by inverted microscopic observation. Apoptosis in the cardiomyocytes was detected by Hoechst 33258 staining and fluorescence microscopy. The levels of lactate dehydrogenase (LDH) and superoxide dismutase (SOD) in the cell culture supernatants, and the reactive oxygen species (ROS) in the cells were also measured by microplate reader. The protein levels of PKC, p-p38 MAPK and HSP70 in the cells were detected by Western blotting.RESULTS: Compared with normal group, the cell viability and beating frequency were decreased in H/R group. LDH and ROS contents, apoptotic rate and p-p38 MAPK level increased significantly (P<0.01). Compared with H/R group, PFC preconditioning increased beating frequency, SOD activity and the protein level of PKC and HSP70, and decreased ROS production, the protein level of p-p38 MAPK and cell apoptotic rate. However, the effect of PFC was inhibited by chelerythrine or SB203580.CONCLUSION: PFC may protect cardiomyocytes from hypoxia/reoxygenation injury. Its mechanism is possibly involved in the inhibition of ROS via increasing the activity of SOD and the activation of PKC, and suppression of excessive activation of p38 MAPK.     

Total saponins of Panax ginseng promote hematopoiesis in mice with aplastic anemia

AIM: To observe the effects of total saponins of Panax ginseng (TSPG) on the promotion of hematopoiesis and to explore the underlying mechanism in treating aplastic anemia (AA) in a mouse model.METHODS: For preparation of AA model, BALB/c mice were exposed to sublethal dose of 5.0 Gy γ radiation, followed by transplantation of lymphocytes from DBA/2 donor mice. The experiment was divided into 6 groups, including normal control group, AA model group, TSPG treatment groups with low, medium and high doses, and positive control group with cyclosporine A (CsA). Both TSPG and CsA were administered by gastrogavage. After 15 d treatment, the peripheral hemogram was tested, the cytokine contents in serum were measured, and bone marrow semisolid culture of colony-forming assay was conducted for determining hematopoietic progenitor cells. The protein levels of extracellular signal-regulated kinase 1/2 (ERK1/2) and its phosphorylation status in the bone marrow cells were determined.RESULTS: Curative effect of TSPG in treating AA mice was satisfactory. Peripheral counts of white blood cells and platelet, and concentration of hemoglobin in TSPG groups with medium and high doses were significantly higher than those in model control. TSPG increased the colony numbers of CFU-E, BFU-E, CFU-GM and CFU-MK derived from hematopoietic progenitor cells. Meanwhile, up-regulation of the phosphorylated ERK1/2, decreased contents of Th1 cytokines and increased contents of Th2 cytokines in the serum were observed.CONCLUSION: TSPG possess the dual efficacies on the promotion of hematopoiesis and immunoregulation in AA mice by regulating the expression of Th1/Th2/Th17 cytokines and increasing the phosphorylation of ERK1/2.     

Inhibitory effect of hypoxia preconditioning on hypoxia/reoxygenation-induced apoptosis in cardiomyocytes

AIM: To study the role of hypoxia preconditioning (HP) in hypoxia-reoxygenation (HR)-induced apoptosis in neonatal rat cardiomyocytes and the possible mechanisms. METHODS: Cultured neonatal rat cardiomyocytes were divided into three groups: normal group, HP+H/R group and H/R group. Acridine orange (AO) staining was performed to detect morphological changes of apoptotic cells. Apoptosis rates of cardiomyocytes were detected by flow cytometry. Colorimetric assay was used to detect caspase-3 activity. Expression of Bcl-2 protein was detected by immunohistochemistry combined with computer image analysis. RESULTS: Apoptotic cells were detected by AO staining after hypoxia of 6 h followed by 3 h-reoxygenation. The hypodiploid apoptotic peak was detected by flow cytometry with the apoptotic rates of (29.7±5.4)%. A significantly reduced apoptotic rates of (7.8±1.3)% was detected in HP group（P＜0.01）. The caspase-3 relative activity of cardiomyocytes induced by H/R was 5.9±0.8, significantly higher than that of control group. HP markedly reduced caspase-3 relative activity to 2.6±0.5 in contrast with H/R group （P＜0.01）. Bcl-2 protein was positive in normal cardiomyocytes with an A value of 119.4±7.1. The A value of H/R group was 99.6±5.0, significantly lower than that in normal group （P＜0.01）. The A value of HP+H/R group was 126.5±6.2, significantly higher than that in H/R group（P＜0.01）. CONCLUSION: HP inhibits H/R-induced apoptosis of cardiomyocytes by improving the expression of Bcl-2 and reducing caspase-3 activity.     

Panax quinquefolium saponin attenuates ventricular remodeling after acute myocardial infarction in rats by inhibiting endoplasmic reticulum stress-related apoptosis

AIM: To investigate the effect of Panax quinquefolium saponin (PQS) on ventricular remodeling after acute myocardial infarction (AMI) in rats and its mechanism. METHODS: Ninety healthy male SD rats were randomly divided into sham group, AMI group, taurine 300 mg·kg-1·d-1 group, PQS 50 mg·kg-1·d-1 group, PQS 100 mg·kg-1·d-1 group and PQS 200 mg·kg-1·d-1 group. AMI models were produced by ligating the left coronary arteries in SD rats. The rats in each treatment group were gavaged with drugs dissolved in water (10 mL·kg-1·d-1), and the rats in sham group and AMI group received equal volume of water. Four weeks after MI, the left ventricle fractional shortening, ejection fraction and structure were evaluated by echocardiography. Myocardial infarct size was measured by 2,3,5-triphenyltetrazolium chloride staining. The hydroxyproline level was measured by colorimetric method. Apoptosis of the cardiomyocytes was detected by TUNEL. In addition, the expression of endoplasmic reticulum stress-related molecules in the noninfarcted myocardium was determined by Western blotting. RESULTS: Compared with AMI group, the left ventricular end-systolic dimension in PQS 50 mg·kg-1·d-1 group, PQS 100 mg·kg-1·d-1 group and PQS 200 mg·kg-1·d-1 group decreased by 17.2%, 20.3% and 38.8% respectively,and the left ventricular end-diastolic dimension decreased by 8.91%, 8.95% and 17.20%, respectively.The left ventricular end-systolic volume decreased by 31.4%, 38.5% and 67.0%, respectively, and the left ventricular end-diastolic volume decreased by 18.2%, 18.8% and 34.2%, respectively.The left ventricular ejection fraction increased by 44.9%, 60.1% and 118.0%, respectively,and the fractional shortening increased by 55.4%, 71.0% and 148.0%, respectively.The infarction size decreased by 4.6%, 39.5% and 55.8%, respectively,and the hydroxyproline level in noninfarcted myocardium decreased by 34.5%, 35.9% and 48.7%, respectively. Compared with AMI group, the myocardial apoptotic index in PQS 200 mg·kg-1·d-1 group decreased by 27.3%, the protein expression of Bcl-2 increased by 114.0%, and that of Bax, GRP78, CRT and CHOP decreased by 53.1%, 79.9%, 80.8% and 42.5%, respectively. The above mentioned protective effects in PQS 200 mg·kg-1·d-1 group and taurine group were similar. The Spearman correlation analysis revealed that CHOP expression had significant positive correlation with apoptotic index (r=0.797, P<0.01). CONCLUSION: PQS attenuates ventricular remodeling in rats. The underlying mechanism may be associated with the inhibition of CHOP-mediated endoplasmic reticulum stress-related cardiomyocyte apoptosis.     

Injury pathways of hypoxia/reoxygenation in AC16 cardiomyocyte

AIM:To investigate the effects of hypoxia/reoxygenation (H/R) for different reoxygenation times on cardiomyocyte injury. METHODS:Human cardiomyocyte AC16 was cultured in glucose-free and serum-free DMEM with 1% O₂ for 24 h, 10% fetal bovine serum and low glucose DMEM combined with 21% O₂ were used to establish reoxygenation for 2 h, 6 h and 12 h, respectively. The cell viability was measured by CCK-8 assay. The protein levels of different cell injury pathway related molecules, such as LC3-Ⅱ/-I (autophagy), caspase-1 and gasdermin D (pyroptosis) and caspase-3 and Bax/Bcl2 (apoptosis), were determined by Western blot. RESULTS:Compared with blank control group, the cell viability in each H/R group was continuously decreased with the extension of reoxygenation time (P<0.05). The expression of LC3-Ⅱ/-I was up-regulated in hypoxia group and H/R group compared with blank control group (P<0.05). In addition, the protein levels of cleaved caspase-1 and cleaved gasdermin D were increased in H/R groups for 6 h and 12 h, respectively (P<0.05). Cleaved caspase-3 and Bax/Bcl2 were increased after reoxygenation for 12 h (P<0.05). CONCLUSION:Autophagy in hypoxia-induced AC16 cells is up-regulated, and then decreased by reoxygenation. The cell pyroptosis is activated earlier than the apoptosis during reoxygenation.     

Effects of acetal hairy holly extractive compound R4 on rat cardiomyocyte injury induced by hypoxia/reoxygenation

AIM: To observe the effects of acetal hairy holly extractive compound R4(AHHECR4) on myocardial cell injury induced by hypoxia/reoxygenation. METHODS: The model of rat myocardial cell injury was induced by hypoxia/reoxygenation. The activity of superoxide dismutase (SOD) in the myocardial cells was measured by the method of xanthine oxidase. The content of malondialdehyde (MDA) was determined by the method of thiobarbituric acid. The activity of dehydrogenase (A) in mitochondria was detected by MTT assay. The activity of lactate dehydrogenase(LDH) and the content of NO in the culture medium were also evaluated. RESULTS: AHHECR4 at concentrations of 5, 10 and 20 μmol/L remarkably increased SOD activity and the value of A, and significantly inhibited MDA production and LDH leakage. Greatly increased content of NO in the culture medium was also observed. CONCLUSION: The results indicate that AHHECR4 has a protective effect on myocardial cells under the condition of hypoxia/reoxygenation injury.     

Fuzi polysaccharide protects neonatal rat cardiomyocytes with hypoxia-reoxygenation by inhibiting endoplasmic reticulum stress

AIM: To investigate whether the protection mechanism of Fuzi polysaccharide (FPS) is related to inhibition of endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R). METHODS: Cultured rat myocardial cells were divided into control group, H/R group (hypoxia for 3 h and reoxygenation for 6 h) and different concentrations of FPS (0.1 g/L, 1 g/L, 10 g/L or 20 g/L) +H/R groups. The cell survival was detected by MTT assay and cell apoptosis of cardiomyocytes was measured by flow cytometry using Annexin V-FITC staining. The expression of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase-12 were determined by Western blotting. The mRNA expression of CHOP and caspase-12 was detected by quantitative PCR. RESULTS: After reoxygenation, the expression of GRP78, CHOP and caspase-12 in cardiomyocytes was increased. Compared with H/R group, the expression of GRP78, CHOP and caspase-12 in FPS+H/R groups was significantly inhibited, the survival rate of cardiomyocytes was increased and the apoptosis of cardiomyocytes was inhibited. This protective effect of FPS was in a dose-dependent manner and reached its peak at 10 g/L. CONCLUSION: Fuzi polysaccharide protects cardiomyocytes from H/R injury. The mechanism is related to inhibiting endoplasmic reticulum stress.     

Effects of Panax notoginseng saponins on PCSK9-LDLR expression and blood lipid metabolism in golden hamsters

AIM: To explore the regulatory effect of Panax notoginseng saponins (PNS) on hyperlipidemia in golden hamsters and its mechanism. METHODS: The hamsters (n=30) were randomly divided into 3 groups:normal group, model group, and PNS group. The animals in normal group was given common feed. The animals in other groups were given high-fat diet to construct a hyperlipidemia model. After induction for 4 weeks, the drugs were given by intraperitoneal injection for another 12 weeks. After the last drug given, the serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured by biochemical tests. The distribution and expression of proprotein convertase subtilisin/kexin type 9 (PCSK9) and low-density lipoprotein receptor (LDLR) in liver were detected by real-time PCR, immunohistochemistry and Western blot. RESULTS: Compared with normal group, the serum levels of TC, TG, LDL-C and ALT in model group were increased significantly (P < 0.05). The expression of PCSK9 was increased, while the protein level of LDLR was decreased (P < 0.05). Compared with model group, the levels of TC, TG, LDL-C and ALT in PNS group were decreased significantly (P < 0.05), PCSK9 was mainly distributed in cytomembrane with decreased expression, and LDLR was mainly distributed in the cell membrane and plasma with increased expression. HDL-C and AST had no significant change during this time. CONCLUSION: Panax notoginseng saponins reduces the blood lipid levels in golden hamsters, which may be related to the regulation of PCSK9-LDLR signaling pathway.