L-Carnitine inhibits H2O2-mediated NFATc3 nuclear translocation

AIM:To explore the effect of L-carnitine on nuclear factor of activated T-cells,cytoplasmic 3 (NFATc3) in cardiomyocytes under H2O2 stimulation. METHODS:Primary cultured neonatal rat myocardial cells were stimulated by H2O2 at concentration of 200 μmol/L for 12 h to induce oxidative stress injury. In treatment group, L-carnitine and cyclosporin A (CsA), a specific inhibitor of calcineurin (CaN), were administered 30 min prior to H2O2 stimulation. After treatment, total, cytoplasmic and nuclear NFATc3 protein levels were determined by Western blotting. The method of immunofluoresence was used to evaluate the distribution of NFATc3. RESULTS:H2O2 treatment produced no effect on the expression of total NFATc3, but caused its translocation from the cytosolic to nuclear compartment, which was greatly blunted by L-carnitine pretreatment. CONCLUSION: L-carnitine antagonized oxidative stress injury via alleviating NFATc3 nuclear translocation.     

Aortic expression of HSP22, TNF-α and eNOS in rats with hyperlipidemia and effects of atorvastatin

AIM:To establish a rat hyperlipidemia model for studying the aortic expression of heat shock protein 22 (HSP22), tumor necrosis factor alpha (TNF-α) and endothelial nitric oxide synthase (eNOS) and the effect of atorvastatin intervention. METHODS:Hyperlipidemia model was established in SD rats. Afterwards, the rats were divided into normal control group, high fat group and high fat+atorvastatin intervention group. The expression of HSP22 and TNF-α in the rat aortas was detected by immunohistochemical assay and the expression of eNOS was assessed by Western blotting. RESULTS:No detectable expression of HSP22 and TNF-α in the normal control group was observed. However, the expression of HSP22 and TNF-α was positive in the high fat group and the atorvastatin intervention group. The mean densities of HSP22 and TNF-α positive particles were significant lower in the atorvastatin intervention group as compared with high fat group (both P＜0.05). The expression of eNOS protein in the high fat group and atorvastatin intervention group was significantly lower than that in normal control group (P<0.01). However, no marked difference of eNOS protein expression between high fat group and atorvastatins intervention group was observed. CONCLUSION: The expression of HSP22 and TNF-α in the rat aortas is increased in the hyperlipidemia rat model. This effect can be restored by atorvastatin treatment. The expression of eNOS in the rat aortas is decreased in the hyperlipidemia rat model, but this tendency could not be attenuated by atorvastatin.     

Hydrogen sulfide ameliorates high glucose-induced endothelial cell senescence by suppressing oxidative stress

AIM：To explore the effect of hydrogen sulfide on the senescence of human umbilical vein endothelial cells (HUVECs) induced by high glucose. METHODS：Senescence model was established by treating HUVECs with 33 mmol/L glucose for 48 h. The parameters were detected to demonstrate the effect of hydrogen sulfide on senescence and the mechanism involved was also investigated. RESULTS：In the cells treated with high glucose, the proliferation was attenuated with a higher number of senescence-associated β-galactosidase (SA-β-Gal) positive cells, and plasminogen activator inhibitor 1 (PAI-1) protein expression, malondialdehyde (MDA) production and NF-κB p65 activity were increased significantly, but the expression of superoxide dismutase 1 (SOD1) was decreased. However, the cell number and SOD1 expression were increased, and the number of SA-β-Gal positive cells, PAI-1 protein expression, MDA production and the activity of NF-κB p65 were decreased after sodium hydrosulfide (100 and 200 μmol/L) treatment.CONCLUSION：Exo-genous hydrogen sulfide prevents HUVECs against high glucose-induced senescence by suppressing oxidative stress and NF-κB p65 activity.     

Mechanisms of hyperglycemia induced by immunosuppressant FK506

AIM：To investigate the effect of immunosuppressant FK506 on serum glucose in rats and to explore its mechanism. METHODS：Sprague-Dawley rats (n=12) were randomly divided into drug group and normal group. The rats in drug group were intraperitoneally injected with FK506 at dose of 1 mg·kg-1·d-1 and the rats in normal group received saline (1 mL·kg-1·d-1, ip) for 14 d. The fasting weight and fasting glucose were regularly measured every 2 d. Visceral fat was isolated from the rats at the end of experiment. The mRNA expression of adiponectin, leptin, visfatin, resistin, retinol-binding protein 4 (RBP4) and peroxisome proliferator-activated receptors γ (PPAR-γ) was determined by real-time fluorescence quantitative PCR. The protein expression of PPAR-γ and adiponectin was measured by Western blotting. RESULTS：Compared with normal group, the concentration of fasting blood glucose in model group was significantly increased from the 10th day (P<0.05). At day 14, the fasting blood glucose of the model group increased from (5.10±062) mmol/L to (7.73 ± 0.73) mmol/L. No significant change of blood glucose in normal group between the 10th day and the 14th day ［from (4.66 ± 0.32) mmol/L to (5.80±0.10) mmol/L］ was observed. Compared with normal group, the mRNA expression of PPAR-γ, adiponectin and leptin in the adipose tissue of model group was significantly decreased (P<001), whereas the expression of visfatin, resistin and RBP4 was significantly increased (P<005). Compared with normal group, the expression of PPAR-γ and adiponectin in model group was decreased (P<001). CONCLUSION：FK506 may decrease the expression of PPAR-γ to change the expression of adipocytokines and induce hyperglycemia in rats.     

Expression of TMEM16A as a calcium-activated chloride channel in Fischer rat thyroid follicular epithelial cells and its electrophysiologic pro-perties

AIM：To investigate the expression of transmembrane protein 16A(TMEM16A) in Fischer rat thyroid follicular epithelial (FRT) cells and its electrophysiologic properties. METHODS：The eukaryotic expression vector of pUB6/V5-TMEM16A was constructed and transfected into FRT cells by liposome-mediated transfection. In order to obtain the high efficiency of gene transfection and expression, the quantity and ratio of lipid/DNA complexes were optimized. The FRT cells stably expressing TMEM16A were gained by the selection with blasticidin and confirmed by the techniques of RT-PCR and immunofluorescence. The expression and location of TMEM16A in the FRT cells were observed under an inverted fluorescence microscope. TMEM16A protein was associated with calcium-dependent chloride current, as measured with halide-sensitive fluorescent protein and patch-clamp technique. RESULTS：The results of double digestion and sequencing indicated that TMEM16A was cloned into pUB6/V5. The results of RT-PCR and immunofluorescence confirmed that TMEM16A was expressed in the FRT cells after transfection with TMEM16A. The classical calcium-activated chloride channel currents were recorded in the FRT cells stably expressing TMEM16A by the technique of patch-clamp and halide-sensitive fluorescent protein YFP-H148Q/I152L. CONCLUSION：The protein expression of TMEM16A in the FRT cells was observed. TMEM16A is the molecular identity of calcium-activated chloride channels.     

Effects of Kv1.5 on proliferation and apoptosis of rat PASMCs under hypoxia+hypercapnia condition and relationship with MAPK pathway

AIM：To investigate the effects of voltage-dependent K＋ channel 1.5 (Kv1.5) on the proliferation and apoptosis of rat pulmonary artery smooth muscle cells (PASMCs) under hypoxia+hypercapnia condition and the relationship with mitogen-activated protein kinase(MAPK) signal pathway. METHODS：The PASMCs isolated from the male SD rat were cultured under hypoxia+hypercapnia condition, and randomly divided into normal group (N group), hypoxia+hypercapnia group (HH group), hypoxia+hypercapnia+DMSO incubation group (HD group), hypoxia+hypercapnia+U0126 (an extracellular signal-regulated kinase 1/2 inhibitor) incubation group (HU group), hypoxia+hypercapnia+SB203580 (a p38 mitogen-activated protein kinase inhibitor) incubation group (HS group), and hypoxia+hypercapnia+anisomycin (an agonist of MAPK) incubation group (HA group). Cell Counting Kit-8 was used to detect the cell viability. The protein expression of Kv1.5, PCNA and Bax was detected by Western blotting. RESULTS：Compared with N group, the cell viability and PCNA protein expression in HH group and HD group were significantly raised (P<001), but Kv1.5 and Bax proteins were significantly decreased (P<0.01). No difference between HH group and HD group was observed (P>005). Compared with HD group, the cell viability and PCNA protein expression in HU group, HS group and HA group were decreased (P<0.05 or P<0.01), but Kv1.5 protein and Bax protein were raised (P<0.01), with the most significant changes in HA group. ^{CONCLUSION：}The regulation of Kv1.5 to the proliferation and apoptosis of PASMCs under hypoxia+hypercapnia condition might have a relationship with the activation of MAPK signal pathway.     

番茄新品种潍科粉3 号的选育

潍科粉3 号是以H10A 为母本,以J10211 为父本杂交选育而成的粉果番茄一代杂种。早熟,由定植到第1 穗果成
熟需75 d（天）左右,植株长势强,无限生长类型,连续坐果能力强,始花节位在第6～7 节;果实略高圆形,着色均匀,
亮粉色,果实味浓爽口,风味佳,VC 含量高达256 mg·kg-1;硬度高,萼片平展,商品性好,单果质量230～250 g,每
667 m² 产量13 000 kg 以上;对番茄黄化曲叶病毒、疫病、叶霉病的抗性较对照梦之粉强。适于温室和大棚早春、秋延后及
越冬栽培。     

不同时期接种AM 真菌对大棚黄瓜产量及品质的影响

研究不同时期接种丛枝菌根真菌根内球囊菌（Glomus intraradices,GI）对大棚土壤栽培黄瓜植株生长、产量及营
养品质的影响。结果表明：黄瓜不同时期接种GI 对其生长均有促进作用,与不接菌的对照相比,播种时接菌和移栽时接菌处理使黄瓜的单株产量分别提高54%、34%;播种时接菌处理的黄瓜叶片的叶绿素含量比对照显著提高了14.7%～17.7%;播种时接菌和移栽时接菌的黄瓜硝酸盐含量较对照分别下降了9.4% 和15.0%,总糖含量分别比对照提高了8.9% 和7.1%;移栽时接菌处理的黄瓜粗蛋白含量比对照提高了4.6%;播种时接菌和移栽时接菌显著提高了黄瓜VC 含量。表明接种GI 对黄瓜生长和产量品质具有一定的改善作用。     

厚皮甜瓜新品种敦蜜1 号的选育

敦蜜1 号是以自交系ML29 为母本,以自交系ML20 为父本配制而成的厚皮甜瓜一代杂种。中早熟,露地栽培生育
期87 d（天）左右。果实发育期40 d（天）左右。植株生长势强,叶色深绿。果实椭圆形,果形指数1.4,果皮纯白色带网纹,
果肉浅绿色,肉厚3.4 cm,中心可溶性固形物含量16.4%,耐贮运。单瓜质量1.5 kg 左右,每667 m² 产量2 260 kg 左右。抗
甜瓜蔓枯病、霜霉病、白粉病。适宜于酒泉市及类似区域大田地膜覆盖种植。     

马铃薯新品种天薯12 号的选育

天薯12号是以品系天97-8-98为母本,庄薯3号为父本杂交选育而成的马铃薯新品种。从出苗至块茎成熟126 d（ 天）
左右,属晚熟品种。薯块椭圆形,黄皮黄肉,芽眼浅而紫。单株结薯4.1 个,平均单薯质量105 g,大中薯率87.4%。每667 m²
产量在1 500 kg 以上,适于甘肃天水、临夏、定西、平凉、陇南等地种植。