黄瓜CsSUN和CsLNG1调控果实大小的机理分析

对黄瓜Q30(CsSUN/CsLNG1)及以其为遗传背景的3个近等基因系材料,即Q30(CsSUN/CsLNG1)、QK1.2-S(Cssun/CsLNG1)、QK2.1-S(CsSUN/Cslng1)、QK1.2+2.1-S(Cssun/Cslng1)进行组织形态、内源激素和转录水平的分析结果表明:与QK1.2-S和QK2.1-S相比,Q30果实最为细长,茎粗最小,植株最高。在果实各发育期,Q30的细胞最小,而细胞密度最大。Q30在开花前6 d的BR/ABA及GA3/ABA显著低于3个近等基因系,随着果实发育差异逐渐缩小。各材料ZT/ABA和IAA/ABA在果实发育各时期基本无显著差异。开花前6d和开花当天Q30的CsSUN表达量均显著高于QK1.2-S和QK1.2+2.1-S,Cs LNG1表达量显著高于QK1.2-S,整体来看也高于QK1.2+2.1-S;与细胞膨胀相关的基因Csa1G422480 (木葡聚糖内转葡糖基酶基因)、 Csa6G014540 (扩张蛋白基因)、 BR生物合成基因Csa1G524640和GA3调节基因Csa3G872170的定量分析结果却相反,在子房期Q30中的表达量显著低于3个近等基因系。随着果实发育,Q30的CsSUN表达水平与QK1.2-S和QK1.2+2.1-S差异逐渐缩小,CsLNG1与QK2.1-S和QK1.2+2.1-S差异也逐渐缩小,而Csa1G422480、Csa6G014540、Csa1G524640、Csa3G872170表达水平反而逐渐上升,后期甚至显著高于3个近等基因系。综上所述,CsSUN和Cs LNG1控制Q30黄瓜细长果实是由于子房期抑制了细胞增大,导致细胞体积小,细胞密度增大;进入果实迅速增长期后该基因对细胞大小的抑制作用减弱,在原有数量基础上细胞逐渐变大,果实持续增长。     

外源ALA缓解ABA抑制草莓根系伸长生长的机理研究

以栽培草莓‘红颜’（Fragaria×ananassa Duch.‘Benihoppe’）为材料，探讨5–氨基乙酰丙酸（ALA）与脱落酸（ABA）以及生长素（IAA）之间的关系，以期为ALA在草莓生产上应用提供理论依据。结果显示，外源ABA处理抑制草莓根系伸长生长，而ALA缓解ABA的抑制效应。ABA处理降低草莓根尖内源生长素含量，ALA则促进内源ABA含量提高。ABA和（或）ALA处理对草莓根尖ABA生物合成关键基因NCED1、NECD2，以及ABA氧化代谢基因CYP707A的表达没有显著影响。但ABA处理诱导其受体基因PYL4和PYL8以及ABA信号通路关键蛋白激酶基因SnRK2.1、SnRK2.2、SnRK2.3、SnRK2.4、SnRK2.5和SnRK2.6表达上调，而ALA却没此效应，说明ALA-ABA调控草莓根系伸长生长效应不涉及ABA信号途径。另一方面，ABA和（或）ALA处理对IAA合成基因YUC1表达没有影响；ABA处理下调YUC2和YUC3以及IAA内向运输基因AUX1表达，但是这种效应不能被ALA逆转。值得关注的是，IAA外向运输蛋白编码基因PIN1在ABA处理后...     

不同分枝西瓜品种生长过程中内源激素含量的变化

以多分枝西瓜品种陇抗9 号与不分枝西瓜品种无杈早为试材，采用超高效液相色谱串联质谱的分析方法，研究分 析不同分枝西瓜品种生长过程中引哚甲酸（ICA）、引哚乙酸（IAA）、玉米素（Z）、二氢玉米素（DHZ）、脱落酸（ABA） 等内源激素含量的变化。结果显示，在伸蔓期与果实膨大初期，不分枝西瓜品种叶片中ICA、IAA+ICA 含量显著高于多分 枝西瓜品种；在整个生长期，不分枝西瓜品种叶片中Z、DHZ+Z 含量低于多分枝品种；且不分枝西瓜品种的（ICA+IAA）/ （Z+DHZ）、（ICA+IAA）/ABA、（ICA+IAA）/（GA1+GA3+GA4+GA7）在伸蔓期与果实膨大初期显著高于多分枝品种。由此 可见，较高含量的ICA 对西瓜侧枝的分生有抑制作用，较高含量的Z 与DHZ 对西瓜侧枝的形成有促进作用；（ICA+IAA）/ （Z+DHZ）、（ICA+IAA）/ABA、（ICA+IAA）/（GA1+GA3+GA4+GA7）的较高比值不利于西瓜侧枝的形成。     

喷施GA3和2,4-D对留树保鲜脐橙落果和内源激素含量的影响

 以纽荷尔脐橙（Newhall Navel Orange）为试材,测定喷施GA₃和2,4-D的植株留树保鲜果实的落果率和果实内源赤霉素（GA）、生长素（IAA）、玉米素核苷（ZR）、脱落酸（ABA）含量的变化,探讨内源激素与留树保鲜脐橙落果的关系。结果表明：植物生长调节剂处理能降低果实内源GA、IAA、ZR含量下降的速度,减缓内源ABA及ABA/（GA + IAA + ZR）的升高,减少留树保鲜过程中的落果,其中以20 mg · L^-1 GA₃ + 20 mg · L^-1 2,4-D混合处理的效果最好,且留树保鲜应以60 d左右为宜。初步分析认为内源GA、IAA、ZR含量的下降,内源ABA及ABA/（GA + IAA + ZR）的升高加速了果实离层的产生,共同促进了留树保鲜脐橙果实的衰老脱落。     

‘金煌’杧果胚正常与胚败育果实内源激素的变化

 研究了‘金煌’杧果果实发育前期内源激素变化与胚胎败育的关系。结果表明：胚胎败育在坐果后30 d完成,20 ~ 30 d为胚发育的关键时期,胚败育果实与胚正常果实大小差异主要缘于果肉的差异。在果实发育初期,败育胚的IAA、ABA含量高于正常胚,GA₃和ZT含量低于正常胚。胚败育果实的果肉中GA₃含量低,而ZT含量高于胚正常果实果肉,IAA和ABA的含量在后期也高。胚中高含量的GA₃、ZT和低含量的ABA有利于胚正常发育。胚中ZT的下降和ABA的持续增加以及（GA₃ + IAA + ZT）/ABA的比值小于其果肉中的比值,是导致胚胎败育的重要因素;在果实发育中,胚胎的败育和胚胎与果肉中（GA₃ + IAA + ZT）/ABA均低是导致胚败育果实小的重要原因。     

LED补光组合对大棚越橘生长发育的影响

以2年生南高丛越橘‘Emerald’为材料，以大棚内自然光作为对照，研究LED光源的红蓝光（3︰1和6︰1）、紫外光（UVA）对植株长势、叶片光合作用、碳氮代谢、开花基因表达及开花率、果实品质的影响。结果表明：红蓝光组合处理下‘Emerald’的植株营养生长较旺盛，株高、1年生枝条长度和粗度显著高于对照。此外，红蓝光（6︰1）处理下叶片的叶绿素相对含量、比叶重和净光合速率均显著提高。红蓝光组合也可诱导植株开花，开花基因FT表达量和开花率明显高于对照。紫外光下叶片的氮含量、开花率及FT基因表达量显著高于对照。不同光质组合补光对‘Emerald’的果实品质有显著影响，红蓝光（3︰1）处理下果实的质量、横纵径、可溶性固形物、可溶性糖、花青素含量和糖酸比均高于对照。总之，不同光质补光会促进越橘‘Emerald’的生长发育，红蓝光6︰1组合对促进营养生长作用相对较大，红蓝光3︰1组合对提高果实品质效果较好。紫外光虽能改变植株形态和促进开花，但果实品质提高效果较红蓝光处理稍弱。     

番茄果胶裂解酶基因SlPL参与调控裂果机制研究

以裂果率差异极显著的番茄为材料,分析了SlPL(Solyc03g111690)基因的表达差异,进一步利用基因遗传转化对其进行功能验证。结果表明,SlPL在易裂番茄‘NT189’中的表达量显著高于耐裂番茄‘NT91’;在番茄果实中的表达量显著高于根、茎、叶、花等器官,且在果实转色期和红熟期表达量较高;通过灌水处理和ABA处理诱导果实开裂,发现在相同处理时期,易裂果材料果实中SlPL表达量总体显著高于耐裂果材料。通过遗传转化获得SlPL过表达（OEPL）和敲除（pl）的株系,与野生型相比,OEPL更易裂果,且果实硬度显著降低,pl果实硬度升高。OEPL果实中原果胶含量显著低于野生型,水溶性果胶含量显著高于野生型,pl果实中原果胶和总果胶含量显著高于野生型;OEPL果实中果胶裂解酶活性显著高于野生型,pl果实中果胶裂解酶活性显著低于野生型。基因表达分析发现,OEPL果实中细胞壁代谢相关基因SlPG2、SlPME2.1、SlCel2、SlGH9C5和乙烯合成途径相关基因SlACS4、SlACO1的相对表达量显著高于野生型,pl果实中则相反。pl果实中乙烯响应因子SlERF2的相对表达量显著高于...     

H2S与ABA缓解低温胁迫对黄瓜幼苗氧化损伤的交互效应

为了探明硫化氢（H2S）与脱落酸（ABA）在提高植物耐冷性中的互作关系,以黄瓜幼苗为试材,叶面分别喷施1.0 mmol · L-1硫氢化钠（NaHS,H2S供体）、0.15 mmol · L-1次牛磺酸（HT,H2S清除剂）、50 μmol · L-1ABA、3 mmol · L-1 Na2WO4（钨酸钠,ABA合成抑制剂）、3 mmol · L-1 Na2WO4 + 1.0 mmol · L-1 NaHS、0.15 mmol · L-1 HT + 50 μmol · L-1 ABA及去离子水（H2O）,研究低温（8 ℃昼/5 ℃夜）胁迫下H2S和ABA对黄瓜幼苗活性氧积累及抗氧化系统的影响。结果表明,低温胁迫48 h,NaHS和ABA预处理的幼苗冷害指数显著降低。ABA可以提高L–/D–半胱氨酸脱巯基酶（LCD/DCD）活性及其基因表达量,促进内源H2S产生;NaHS处理的9–顺式–环氧类胡萝卜素双加氧酶（NCED）活性及其基因相对表达也明显增加,内源ABA含量快速升高。低温下NaHS和ABA处理均可减少活性氧积累,提高超氧化物歧化酶（SOD）、过氧化物酶（POD）、抗坏血酸过氧化物酶（APX）和谷胱甘肽还原酶（GR）活性与基因相对表达量,增加抗坏血酸（AsA）和谷胱甘肽（GSH）含量及还原型/氧化型抗坏血酸（AsA/DHA）和还原型/氧化型谷胱甘肽（GSH/GSSG）比例,从而减轻低温胁迫对黄瓜幼苗的过氧化伤害。ABA合成抑制剂Na2WO4处理后,H2S对黄瓜幼苗抗氧化能力的促进效应明显减弱;同样,ABA对黄瓜幼苗活性氧的调控作用也被H2S清除剂HT所逆转。可见,H2S和ABA可诱导黄瓜幼苗耐冷性,二者在信号转导过程中存在交互效应和“对话”机制。     

苹果类受体激酶基因MdLYK1正调控对腐烂病的抗性

以苹果类受体激酶基因MdLYK1(MD09G1111800)为研究对象，结合生物信息分析、功能验证和表达分析，探究其对抗腐烂病的作用和可能的作用机制。结果表明，MdLYK1与拟南芥类受体激酶基因AtLYK1同源，氨基酸序列的相似性为68.1%。将该基因在‘烟富6号’苹果果实中瞬时过表达后显著提高了果实对腐烂病的抗性。将其导入杜梨悬浮细胞，获得3个过表达细胞系。接种腐烂病菌（Valsa pyri）后，菌落在所有过表达细胞系上的生长速度显著低于野生型细胞。与野生型相比，所有过表达细胞系对Valsapyri代谢物的敏感性显著降低。此外，MdLYK1过表达显著增强了杜梨悬浮细胞病原体相关分子模式触发的免疫反应、活性氧和茉莉酸等信号相关关键基因的上调表达。综上所述，MdLYK1正调控苹果和梨对腐烂病的抗性，且病原体相关分子模式触发的免疫反应、活性氧和茉莉酸等信号参与了其对抗性的调控过程。     

枇杷7个脱水素基因表达差异分析

为进一步明确枇杷（Eriobotrya japonica Lindl.）中不同脱水素基因家族成员（EjDHN）的功能和响应机制,以白沙枇杷品种‘宁海白’为试材,分析了7个EjDHN基因在不同器官、果实发育期及ABA和干旱胁迫条件下的表达模式。结果表明,EjDHN5在各器官中表达量都比较高,EjDHN4主要在花中表达,EjDHN2、EjDHN3、EjDHN6和EjDHN7主要在茎中表达。在果实发育过程中,除EjDHN3外,其他家族成员均与种子发育有关;而EjDHN2和EjDHN5在果肉中表达量较高且与果肉发育有关。7个EjDHN基因在枇杷叶片中的季节性表达变化趋势基本一致,均在冬季表达量最高,而EjDHN1、EjDHN2、EjDHN4和EjDHN5在初夏也有较高的表达量。在干旱胁迫后,叶片中7个EjDHN基因的表达均出现显著增强趋势,其中EjDHN6增幅最大。各基因对ABA处理也有不同响应,以EjDHN6最为敏感。     

CXCL16 deficiency attenuates STZ-induced diabetic nephropathy in mice

AIM: To explore the effect of CXCL16 deficiency on streptozocin (STZ)-induced diabetic nephropathy in mice. METHODS: CXCL16 knockout (C16 KO) mice (8 years old) were used to build up diabetes model by treating with STZ.Age- and gender-matched wild-type (WT) C57BL/6J mice treated with STZ were used as control. All mice were fed with chow diets for 12 weeks, and the development of diabetic nephropathy was evaluated. RESULTS: Compared with the WT mice treated with STZ, C16 KO mice treated with STZ presented lower fasting glucose levels and better glucose tolerance power. C16 KO mice treated with STZ also had lower urine protein levels and smaller areas of glomerular injury as compared with WT mice treated with STZ. Furthermore, CXCL16 deficiency decreased the contents of renal reactive oxygen species (ROS), malondialdehyde (MDA) and oxidized low-density lipoprotein (ox-LDL) and the mRNA expression of lectin-like oxidized low-density lipoprotein receptor 1 (Lox-1), and attenuated the expression of renal inflammatory factors including tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), as well as chemokines including intercellular cell adhesion molecular 1 (ICAM-1) and chemokine C-X-C motif ligand 1 (CXCL1). CONCLUSION: CXCL16 deficiency obviously inhibits the development of STZ-induced diabetic nephropathy in mice.     

Inhibition of Rac1 protects cardiac functions in STZ-induced diabetic cardiomyopathy through decreasing pho-p38 MAPK

AIM: To investigate the effects of Rac1 inhibition on the size of cardiomyocytes and left ventricular functions in diabetic cardiomyopathy. METHODS: Type 1 diabetes was induced in 8-week old C57 mice by streptozotocin (STZ, ip injection). Diabetic mice were treated with NSC23766, a specific inhibitor of Rac1 (STZ+NSC group, n=15) or without treatment (STZ group, n=15). Nondiabetic mice were used to serve as empty control (Con group, n=10) or NSC23766 control (NSC group, n=10). The survival rate, LVHW/BW and left ventricular functions were detected at the end of 8 weeks after induction of diabetes. The expression of ANP, BNP, β-MHC and pho-p38 MAPK in the cardiac tissues were analyzed by real-time RT-PCR and Western blotting, respectively. Hematoxylin and Eosin staining (HE) was used to measure the cell size in the cardiac tissues. RESULTS: The functions of left ventricle were significantly impaired in the diabetic animals with decreased survival rate and increased LVHW/BW, which was accompanied by significant increases in ANP, BNP and β-MHC, and elevated pho-p38 MAPK expression in diabetic hearts. The increased survival rate, improved left ventricular functions and decreased LVHW/BW were observed in the diabetic animals treated with NSC. The mRNA expression of ANP, BNP, β-MHC and pho-p38 MAPK was significantly attenuated in the diabetic hearts by NSC treatment. The size of the cardiomyocytes, which increased in diabetic hearts, was decreased in the NSC-treated diabetic cardiac tissue. CONCLUSION: Rac1 inhibition protects left ventricular functions and attenuates hypertrophy, which is associated with the decrease in pho-p38 MAPK expression in diabetic heart. These data suggest that inhibition of Rac1 might be beneficial to diabetic cardiomyopathy.     

Expression of p-p38 MAPK in partial cerebral tissues after hypoxic-ischemic brain damage in neonatal A2AR knockout mice

AIM： To study the expression of p-p38 MAPK in partial cerebral tissues after hypoxic-ischemic brain damage (HIBD) in the neonatal adenosine A2A receptor knockout (A2AR-/-) mice. METHODS：Base on the modified Rice method, the model of HIBD was established. The total 64 C57/BL6 neonatal mice (7 days old) of A2AR-/-(KO) and corresponding wild type (A2AR+/+, WT) were randomized into sham-operated group and model group. The mice in model group were divided into 3 subgroups： 1 d after HIBD, 3 d after HIBD and 7 d after HIBD (n=8 for each group). The cortex and hippocampal CA1 region were used as the study areas. The neuronal apoptosis was detected using TUNEL assay combined with Nissl staining. The expression of p-p38 MAPK and activated caspase-3 was determined by the method of immunohistochemistry. The KO mice and WT mice were also taken from sham-operated group (SKO and SWT, n=10) and model group (MKO and MWT, n=30) 1 d after HIBD to assess the early neurological behavior. RESULTS：The apoptotic neurons, activated caspase-3 and p-p38 MAPK increased after HIBD and peaked at 1 d after HIBD in the cortex and the hippocampal CA1 region. The apoptotic neurons and the expression of activated caspase-3 in KO mice were significantly higher than those in WT mice at the same time point after HIBD. The expression level of p-p38 MAPK in KO mice were significantly higher than that in WT mice at 1 d and 3 d after HIBD. The expression of activated caspase-3 was positively correlated with the expression of p-p38 MAPK in neonatal mice after HIBD (in the cortex：r=0.957, P<0.01; in the hippocampal CA1 region： r=0.939, P<0.01). CONCLUSION：p-p38 MAPK might be involved in the aggravated neuron apoptosis and brain damage induced by A2AR knockout after neonatal HIBO.     

Effect of CCK-8 on signal mechanisms of IL-12 secretion in LPS-induced mice

AIM:To study the effects of CCK-8 on IL-12 secretion in LPS-induced mice and to investigate the signal transduction mechanisms involving NF-κB and p38 MAPK. METHODS:Female BALB/c mice were induced by LPS in the presence or absence of CCK-8, CCK-A or B receptor antagonist. The productions of IL-12p40 and p70 in the sera, lung and spleen tissues were evaluated by ELISA. Changes of pIκB, p-p38 protein expression and the NF-κB/DNA binding activity were examined by Western blotting and EMSA, respectively. RESULTS:CCK-8 increased the expressions of IL-12p40, p70 in the serum, lung and spleen tissues of LPS-induced mice, inhibited IκB phosphorylation and NF-κB/DNA binding activity, increased p38 phosphorylation. CONCLUSION:CCK-8 increases the production of IL-12 in LPS-induced mice probably via activating p38 MAPK. NF-κB might not mediate the activating effect of CCK-8 on IL-12 production.     

朱顶红无菌苗叶片高效再生体系

以朱顶红（Hippeastrum vittatum）叶片为外植体进行离体培养，具有取材方便、试材充足、成本低等优势，但叶片诱导再生率极低，是朱顶红离体培养的一大难题。本试验中分别以‘花孔雀’和‘黑天鹅’朱顶红无菌苗叶片为外植体，探究了不同植物生长调节剂和不同取材部位对不定芽诱导和继代增殖的影响。结果表明：最佳外植体为 MS 培养基中培养 10 d 形成的幼嫩叶片基部（0.5 cm），在光照 16 h · d-1（光照强度 36 μmol · m-2 · s-1）下，不定芽诱导的最适培养基为 MS + 2 mg · L-1 6-BA + 1 mg · L-1 NAA + 2 mg · L-1 TDZ，两个品种的不定芽均以间接途径发生，其中‘花孔雀’在培养 40 d 后形成愈伤组织，55 d形成不定芽，诱导率可达 69.44%；‘黑天鹅’在培养 45 d 后形成愈伤组织，65 d 形成不定芽，诱导率达到 66.67%；最适体细胞胚诱导培养基为 MS + 2 mg · L-1 6-BA + 1 mg · L-1 PIC，‘花孔雀’和‘黑天鹅’的诱导率分别达到 66.67%和 63.89%；最佳不定芽增殖培养基为 MS + 2 mg · L-1 6-BA + 1 mg · L-1 NAA + 1 mg · L-1 TDZ，‘花孔雀’和‘黑天鹅’的增殖系数分别达到 4.67 和 3.46；在不添加植物生长调节剂的 MS培养基中进行生根培养，30 d 后两个品种的生根率均达到 100%；将生根培养 30 d 的小植株转移至室温条件下放置 3 d，摘去封口膜再驯化 3 d 后，移栽至经高温消毒的草炭︰蛭石（体积比）为 1︰1 的基质中，成活率达到 100%     

Effect of normal mesenteric lymph on multiple organ injury in mice with endotoxic shock

AIM: To observe the effects of normal mesenteric lymph (NML) on the lung, heart and liver injuries and the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) in the mice with endotoxic shock (ES). METHODS: The NML was drained form health male BALB/c mice for the intervention of ES after the removal of cellular constituent. Lipopolysaccharide (LPS, 35 mg/kg) was intraperitoneally injected into the mice for the establishment of ES model. After 60 min of LPS injection, the administration of NML (1/15 of whole blood volume) was performed through the femoral artery in NML+ES group. Meanwhile, the mean arterial pressure (MAP) was monitored during the experiment. At 6 h after intraperitoneal injection of LPS or the corresponding time point, blood samples were harvested from the heart through apical centesis for determination of the biochemical indexes to reflect myocardial and hepatocyte injuries. Simultaneously, the lung, heart and liver tissue specimens from a fixed location were harvested for the observation of histomorphology and the measurement of phosphorylation levels of p38 MAPK, ERK1/2 and JNK. RESULTS: Compared with sham shock (SS) group, MAP in ES group and NML+ES group remarkably decreased at multiple time points after intraperitoneal injection of LPS. However, MAP in NML+ES group at 80 min, 90 min, 190 min, 210 min, 240 min, 250 min, 340 min, 350 min, and 360 min were significantly increased compared with ES group. There were normal structures in the lung, liver and myocardium of the mice in SS group, while the morphological damages of these tissues appeared in ES group. Meanwhile, the damages were attenuated in the mice of NML+ES group. The activities of AST, ALT and CK-MB in the plasma in ES group were remarkably higher than those in SS group. The CK-MB activity in NML+ES group was also increased compared with SS group, and the activities of AST and LDH-1 were lower than those in ES group. At 6 h after LPS injection, the phosphorylation levels of p38 MAPK, ERK1/2 and JNK in the lung tissues were remarkably increased. Meanwhile, no statistical difference of these indexes between the myocardial and hepatic tissues was observed. NML intervention decreased the phosphorylation levels of p38 MAPK in the lung tissues, and p38 MAPK, ERK1/2 and JNK in the myocardial tissues. CONCLUSION: The NML administration alleviates multi-organ injuries and reduces the phosphorylation level of p38 MAPK in the lung tissues in the mice subjected to ES.     

p38 MAPK signaling pathway is involved in the regulation of receptor-mediated endocytosis

AIM: To investigate the role of p38 MAPK signaling pathway in the receptor-mediated endocytosis. METHODS: The effects of p38 MAPK on the receptor-mediated endocytosis were observed by using Alexa 594-conjugated Transferrin, in the presence of p38 specific inhibitor SB203580 or ERK pathway specific inhibitor PD98059, or using p38 knockout techniques. RESULTS: In the process of receptor-mediated endocytosis, p38 was activated by phosphorylation. Furthermore, the receptor-mediated endocytosis was inhibited by pretreatment with SB203580 or p38 knockout, while pretreatment with PD98059 had no effect on this process.CONCLUSION: p38 MAPK signaling pathway plays a role in the regulation of receptor-mediated endocytosis.     

Alteration of p38 MAPK activity in lung tissue in diabetic rats

AIM: To observe the pathologic changes in lung and the role of p38 MAPKinase signal pathways in pulmonary alteration in diabetic rats. METHODS: Diabetic rats were induced by intraperitoneally injected streptozotozin (STZ). After 4 weeks, we observed the pathologic changes in lungs, tested protein kinase C (PKC) activities by isotope in lungs of model rats, tested transforming growth factor (TGF-β₁) by Western blotting and immunohistochemical analysis, and determined the expression of p38 MAPKinase mRNA using in situ hybridization.RESULTS: After STZ administration for 4 weeks, we observed thickened pulmonary capillary basal lamina and increased number of fibre in Diabetes mellitus (DM) rats. TGF-β₁ levels, PKC and p38 MAPK activities were also found increased. CONCLUSION: The increased activities of TGF-β₁ and p38 MAPK suggeste that TGF-β₁ may play an important role in diabetic lung, and hyperglycemia-PKC-p38 MAPK signal pathways may be involved in the pathogenesis of diabetes.     

Secoisolariciresinol diglucoside attenuates renal inflammatory injury of mice induced by chronic intermittent hypoxia via inhibiting TXNIP and activating NLRP3 inflammasome

AIM To investigate the effectof flax lignan/secoisolariciresinol diglucoside （SDG） on the inflammatory damage of kidney induced by chronic intermittent hypoxia （CIH）. METHODS C57BL/6N mice were divided into normal （control） group, model （CIH） group and treatment （SDG） group. The changes of the body weight was recorded. Hematoxylin-eosin （HE） staining was used to observe the morphological alterations in the renal tissues. The levels of serum creatinine and blood urea nitrogen were measured by a biochemical analyzer. Hydroxylamine and thiobarbituric acid methods were used to detect the activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） in the renal tissues. The protein levels of thioredoxin-interacting protein （TXNIP） and nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） were detected by immunohistochemical staining, while those of tumor necrosis factor-α （TNF-α）, interleukin-6 （IL-6） and IL-1β were measured by ELISA. The protein levels of TXNIP, NLRP3, apoptosis-associated speck-like protein containing a CARD （ASC）, caspase-1, IL-1β and IL-18 in the renal tissues were also determined by Western blot. RESULTS No significant difference in the body weight and kidney index among the 3 groups was observed （P>0.05）. HE staining showed the swollen epithelial cells of renal tubules with vesicular degeneration, and irregular glomerular morphological change in CIH group, while SDG treatment attenuated the above changes. Compared with control group, the levels of serum creatinine, TNF-α, IL-6 and IL-1β were significantly increased in CIH group （P<0.05）. The significantly increased expression levels of NLRP3 and TXNIP in the cytoplasm of renal tubular epithelial cells in CIH group were detected by immunohistochemical staining. Compared with control group, the activity of SOD was decreased, the content of MDA was increased in CIH group, and the protein expression levels of TXNIP, NLRP3, ASC, caspase-1, IL-1β and IL-18 were up-regulated and then decreased after SDG treatment （P<0.05）. CONCLUSION SDG attenuates the renal inflammatory damage of the mice induced by CIH, and its mechanism may be associated with the inhibition of oxidative stress and activation of NLRP3 inflammasome.