临床下痫样放电对癫痫患者IGF-1水平的影响

目的观察临床下痫样放电的癫痫患者血清胰岛素样生长因子1（IGF-1）水平,并探讨其临床意义。方法以全身强直阵挛性发作为临床表现的特发性癫痫患者86例,无临床发作均超过3个月,检出临床下痫样放电（放电组）47例,脑电图正常（脑电图正常组）39例。选取性别、年龄与癫痫患者相匹配的健康体检者30例作为对照组。采用放射免疫法测定血清IGF-1的浓度,用脑电图观察痫性放电频率,并计算棘波指数。结果放电组IGF-1浓度[（291.32±99.58）ng/m L]明显高于脑电图正常组[（189.00±75.63）ng/m L]（P〈0.01）;脑电图正常组IGF-1浓度[（189±75.63）ng/m L]和对照组IGF-1浓度[（176.00±65.75）ng/m L]比较无统计学差异（P〉0.05）。放电组棘波指数[（23.95±12.13）次]与血清IGF-1含量呈显著正相关（r=0.459,P〈0.05）。结论临床下痫样放电的癫痫患者血清IGF-1表达上调,机体启动了神经保护机制。     

白花蛇舌草乙醇提取物调控DDR1对大鼠肝癌细胞增殖的影响

目的 探讨白花蛇舌草乙醇提取物对大鼠肝癌细胞增殖的影响及作用机制.方法 选取Wistar大鼠82只,采用小剂量二乙基亚硝铵(DEN)构建大鼠肝癌模型,在动物造模成功后随机分为模型组、低剂量组、中剂量组、高剂量组,各20只.造模成功后1 d,模型组给予乙醇提取物溶剂1 mL/(100 g·d)灌胃处理8周,后三组分别给予...     

银杏叶提取物对糖尿病性脑病大鼠海马细胞凋亡的影响

目的 研究糖尿病性脑病与海马区细胞凋亡的关系以及银杏叶提取物(EGb)治疗的效果和机制. 方法 大鼠分为对照(NC)组、糖尿病性脑病(DM+B)组和EGb治疗(EGb)组,分1个月和3个月两个时间点.水迷宫实验观察行为学改变,免疫组化、RT-PCR检测Bcl-2和Bax蛋白及mRNA的表达,ELISA检测脑组织细胞凋亡的水平. 结果 (1)DM+B_1组已出现学习、记忆功能障碍,DM+B_3组更加加晕,EGb组则明显减轻.(2)DM+B_1、DM+B_3组Bcl-2表达较NC组增加,EGb_1、EGb_3组表达更强.(3)DM+B_1、DM+_3组Bax表达较对照组明显增加,EGb_1、EGb_3组则明显减弱.(4)DM+B_1组脑组织细胞凋亡水平升高,DM+B_3组更加明显,治疗组则显著减轻. 结论 海马区细胞凋亡是糖尿病性脑病发病的重要因素,银杏叶提取物可能通过抑制细胞凋亡而对糖尿病性脑病有保护作用.     

桃金娘叶乙醇提取物对小鼠蓖麻油性腹泻及兔离体空肠平滑肌的影响

目的 探讨桃金娘叶乙醇提取物(RT ext)的抗腹泻活性,并研究其对家兔离体肠平滑肌收缩的影响及其相关作用机制。方法 采用高效液相色谱法分析RT ext的化学成分。在体内实验中,通过小鼠急性毒性实验评估RT ext的安全性;采用蓖麻油诱导小鼠腹泻,测定半固体粪便出现时间及4 h内的排空指数,评价RT ext的抗腹泻作用。在离体实验中,建立家兔空肠平滑肌标本,借助BL-420F生物机能实验系统观察RT ext [0.01～10.00 mg(生药)/ml]对兔离体空肠平滑肌自主收缩的影响和对乙酰胆碱(10μmol/L),氯化钾(60 mmol/L)所致的空肠平滑肌痉挛的解痉作用。结果 在体内实验中,未观察到小鼠出现急性毒性症状;RT ext低、中高剂量可极显著推迟小鼠的半固体粪便产生时间(P<0.001),中、高剂量可显著降低蓖麻油诱导小鼠腹泻的排空指数(P<0.05或P<0.01)。在离体实验中,RT ext浓度依赖性抑制空肠平滑肌的自主收缩,其EC50值为0.68 mg/ml,并能阻断乙酰胆碱和氯化钾引起的收缩,其EC50值分别为0.43和0.13 mg/ml。结论 ...     

枳黄方对急性乙醇性肝损伤大鼠肝脂质过氧化水平的影响及机制

目的探讨枳棋子、大黄水提液（枳黄方）对急性乙醇性肝损伤大鼠（ALD）的保护作用。方法将30只大鼠随机分为A、B、C三组每组10只,其中A组予枳黄方6．0ml／kg灌胃,B、C组予6．0ml／kg生理盐水灌胃;间隔45min后A、B组予56。白酒14ml／kg灌胃,C组予50％葡萄糖14mL／kg灌胃,均为1次／d,连续10d。最后1次灌胃后禁食14h,以2％戊巴比妥钠40mg／kg腹腔注射麻醉大鼠,采集肝组织。羟胺法检测肝脏超氧化物歧化酶（SOD）活力,TBA法检测肝脏丙二醛（MDA）水平;采用RT—PCR技术检测肝脏NADPH氧化酶gp-91phox mRNA及p22phox mRNA表达。结果与B组比较,A组SOD活性显著升高,MDA水平及gp-91phox、p22phoxmRNA表达显著降低。结论枳黄方能对抗ALD大鼠肝脏脂质过氧化,可能机制为降低肝脏NADPH氧化酶gp-91phox mRNA及p22phox mRNA表达。     

银杏叶提取物对SKOV3种植性卵巢癌Bcl-2、Bax的影响

<正>银杏叶提取物(EGb 761)主要应用于心脑血管疾病的防治〔1〕,而近年来的一些研究发现银杏叶提取物对某些肿瘤具有抑制增殖的作用。研究显示EGb 761及内脂B可明显降低乳腺癌细胞增殖〔2〕,给予银杏叶提取物可抑制人结肠癌细胞HT-29增殖〔3〕,银杏叶提取物山奈酚可通过诱导凋亡抑制胰腺癌细胞增殖〔4〕。研究还显示银杏叶提取物明显遏制二乙基亚硝胺(DEN)诱发的肝癌增殖〔5〕以及N-甲基-N'-硝基-N-亚硝基胍     

肝细胞提取物组分S4对肿瘤细胞体外增殖的影响

目的观察肝细胞提取物组分Ｓ４对８株肿瘤细胞增殖的影响．方法采用ＭＴＴ比色法研究不同浓度Ｓ４对８株肿瘤细胞不同时相增殖的影响．结果Ｓ４对７４０２，７７２１，７７０３，Ｈｅｐｅ肝癌细胞作用７２ｈ后ＩＣ５０（ｍｇ／Ｌ）分别为３９，４２，９５和６５．对胃腺癌细胞（ＳＧＣ７９０１）、回盲部腺癌细胞（ＨＣＴ８）、肺腺癌细胞（ＧＬＣ８２）作用７２ｈ的ＩＣ５０分别为１４３，９９和５４．对鼻咽癌细胞（ＣＮＥ２）４８ｈ未显示抑制作用．结论Ｓ４抑制７株肿瘤细胞呈现明显的量效与时效关系，在１ｍｇ／Ｌ～１０ｍｇ／Ｌ浓度范围内及２４ｈ～７２ｈ时限内，抑制作用随剂量增加、时间延长而增强     

银杏叶提取物对糖尿病大鼠学习、记忆及海马血红素加氧酶1表达的影响

目的探讨银杏叶提取物(EGb)对糖尿病大鼠学习记忆及海马血红素加氧酶1(HO-1)表达的影响。方法大鼠腹腔注射链脲佐菌素建立糖尿病模型,6个月后以Morris水迷宫观察其学习记忆能力,以RT-PCR观察大鼠海马HO-1 mRNA的表达,以免疫组织化学法观察海马HO-1蛋白表达。结果大鼠糖尿病6个月后Morris水迷宫成绩下降,海马的HO-1 mRNA表达和蛋白表达水平升高(分别为1．635±0．326 vs 0．978±0．214,7．2±1．7 vs 1．9±0．5,均P＜0．01)；糖尿病EGb干预组(100、50 mg/kg)大鼠较糖尿病大鼠Morris水迷宫成绩提高,HO-1 mRNA表达和蛋白表达水平降低(100 mg/kg：0．954±0．144,2．0±0．8；50 mg/kg：0．988±0．154,2．5±0．6,均P＜0．01)。结论EGb可抑制海马的HO-1表达,提高糖尿病大鼠的学习记忆能力。     

血府逐瘀汤、温胆汤、天麻钩藤饮对SHR大鼠心肌组织TNF-α、IFN-γ、G-CSF、MCP-1表达的影响

目的观察血府逐瘀汤、温胆汤、天麻钩藤饮对自发性高血压(SHR)大鼠心肌组织中TNF-α、IFN-γ、粒细胞集落刺激因子(G-CSF)、单核细胞趋化蛋白-1(MCP-1)等炎性细胞因子表达的影响。方法将50只16周龄SHR大鼠随机分为5组,SHR对照组、卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组各10只;另取10只血压正常的WKY大鼠作为正常对照组。卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组分别给予相应的药物灌胃,SHR对照组、正常对照组给予等量生理盐水灌胃,均2次/d,连续灌胃8周。之后断头处死各组大鼠,取其心脏,采用LiquiChip液相蛋白芯片系统检测大鼠心肌组织TNF-α、IFN-γ、G-CSF、MCP-1等炎性细胞因子。结果用药8周后,天麻钩藤饮组、血府逐瘀汤组、温胆汤组大鼠心肌组织TNF-α、G-CSF、MCP-1等炎性细胞因子的表达水平明显降低,IFN-γ的表达升高,与SHR对照组、正常对照组大鼠用药后相比,P均<0.01;血府逐瘀汤组与天麻钩藤饮和温胆汤组相比,P均<0.05。结论血府逐瘀汤、温胆汤、天麻钩藤饮有一定的抗心肌纤维化作用,其机制可能与抑制大鼠心肌组织中TNF-α、G-CSF、MCP-1的表达和提高IFN-γ的表达有关。     

延龄草提取物对异质性及多因性阿尔茨海默病模型大鼠学习记忆与抗氧化能力的影响

目的探讨延龄草提取物对异质性及多因性阿尔茨海默病(H/MAD)模型大鼠学习记忆与抗氧化能力的影响。方法先腹腔注射D-半乳糖促衰老,再反复结扎双侧颈总动脉致脑缺血,最后大鼠侧脑室一次性注射Aβ1~40制备H/MAD模型。实验设空白组,H/MAD模型组,盐酸多奈哌齐组,延龄草总提物高、中剂量组,水洗脱物高、中剂量组,30%乙醇洗脱物高、中剂量组,60%乙醇洗脱物高、中剂量组,85%乙醇洗脱物高中剂量组。各给药组于术后3 d开始灌胃给药6 d。采用Morris水迷宫测试各组大鼠学习记忆能力,并测定大鼠血清中总抗氧化物(T-AOC)、乙酰胆碱酯酶(TCh E)的含量和超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)的活力。结果与模型组比较,给药各组能明显缩短潜伏期、增加过台次数、在第四象限逗留时间延长,并使大鼠血清中T-AOC含量升高、降低TCh E活力,提高SOD、GSH-Px的活性,降低MDA含量(P0.05,P0.01)。结论延龄草提取物(尤其是85%乙醇洗脱物中剂量、60%乙醇洗脱物高剂量)对H/MAD模型大鼠学习记忆有明显的改善作用,其机制可能与增强T-AOC活力、降低TCh E含量及提高H/MAD大鼠的抗氧化作用相关。     

地龙2号对肝纤维化大鼠uPA和PAI-1蛋白表达的影响

目的研究蚯蚓提取物地龙2号对实验性大鼠肝纤维化的uPA和PAI-1蛋白表达的影响。方法52只雄性Wistar大鼠,随机分成6组:正常大鼠组(N);秋水仙碱对照组(CC);造模同时用秋水仙碱0.1mg.Kg-1.d-1灌胃,假模型组(NC):皮下注射花生油(CCl4),灌单蒸水;模型组对照组(MC):皮下注射CCl4花生油混合物,每日单蒸水灌胃;地龙大剂量组(Eh):造模同时用地龙2号50mg.Kg-1.d-1灌胃;地龙小剂量组(El):造模同时用地龙2号25mg.Kg-1.d-1灌胃。8周末处死大鼠,用免疫组化法检测各组大鼠肝脏组织中uPA和PAI-1的表达情况。结果地龙2号大、小剂量组与模型组相比,uPA和PAI-1的表达均显著降低,且uPA与PAI-1的表达下降呈明显的正相关。结论地龙2号可能通过抑制肝纤维化大鼠肝组织中肝星状细胞(HSC)的活化及抑制uPA、PAI-1的表达发挥抗肝纤维化作用。     

Protective Effects of Nafamostat Mesilate on Liver Injury Induced by Lipopolysaccharide in Rats: Possible Involvement of CD14 and TLR-4 Downregulation on Kupffer Cells

Nafamostat mesilate (NM) is a synthetic protease inhibitor with various biological effects. To determine its effect on liver injury related to sepsis, we investigated the effects of NM on lipopolysaccharide (LPS)-induced liver injury. Wistar rats were allocated into two groups; the NM group underwent intraperitoneal NM administration 30 min before LPS administration, and the control group underwent PBS administration. Serum AST and ALT levels were significantly decreased in NM-treated rats. Reduced levels of TNF-α, IL-1β, and IFN-γ were observed after LPS administration in NM-treated rats. No significant differences were observed in IL-6 levels between the NM and the control group. In contrast, HGF levels were significantly increased only in control rats. NM treatment decreased protein and mRNA levels of TLR-4 and CD14. Our data suggest that NM treatment has protective effects against LPS-induced hepatotoxicity through downregulation of TLR4 and CD14 in liver, which decreased TNF-α, IL-1β, and IFN-γproduction in liver.     

氯沙坦对自发性高血压大鼠糖基化终末产物及其受体诱导的血管损伤的影响

背景晚期糖基化终末产物(AGEs)及其受体 RAGE 系统在糖尿病靶器官损伤的病理过程中起非常重要的作用,有研究报道血管紧张素Ⅱ1型受体拮抗剂(ARB)能减少体内外2型糖尿病动物 AGEs 聚集以及氧化应激反应。目的探讨血管氧化应激与 AGE 水平及其受体 RAGE 及核转录因子(NF-kB)等在高血压血管损伤进程中的变化及氯沙坦对其损伤路径的影响。方法选30周龄自发性高血压大鼠(SHR)随机分为 SHR组、氯沙坦组[30 mg/(kg·d)],WKY 组为对照。干预12周,用放免法测定血浆血管紧张素Ⅱ(AngⅡ)水平;免疫荧光检测血管晚期糖基化终末产物(AGEs)表达;免疫组化法检测血管 RAGE 表达。RT-PCR 检测AT_1mRNA、NF-kB mRNA、NADPH 氧化酶 p47 phox mRNA 表达。结果 12周后,SHR 组的血压稳定在治疗前水平[(222±5)mmHg],氯沙坦组血压降至[(158±4)mmHg],且明显低于 SHR 组(P<0.01);氯沙坦组血浆AngⅡ水平达(67.4±5.4)pg/mL,明显高于 SHR 组[(49.5±4.6)pg/mL,P<0.01];氯沙坦组及...     

脱氢表雄酮对氧化型低密度脂蛋白诱导的平滑肌细胞单核细胞趋化蛋白1表达的影响及其机制

目的观察脱氢表雄酮对氧化型低密度脂蛋白诱导的血管平滑肌细胞分泌单核细胞趋化蛋白1的影响,并探讨其作用机制是否与细胞色素P450芳香酶的催化作用有关。方法使用脂质体转染法将含有细胞色素P450芳香酶基因的质粒和空白对照质粒分别转染至体外培养的血管平滑肌细胞,24h后给予氧化型低密度脂蛋白诱导及脱氢表雄酮刺激,采用逆转录聚合酶链反应、实时荧光定量聚合酶链反应及酶联免疫吸附法检测转染后各组细胞单核细胞趋化蛋白1的基因和蛋白表达水平。结果与氧化型低密度脂蛋白刺激组比较,给予氧化型低密度脂蛋白和脱氢表雄酮后单核细胞趋化蛋白1的分泌明显降低(P<0.05)。转染含有细胞色素P450芳香酶基因的质粒组和空白对照质粒组单核细胞趋化蛋白1的分泌差别不明显(P>0.05)。结论脱氢表雄酮能抑制氧化型低密度脂蛋白诱导的血管平滑肌细胞单核细胞趋化蛋白1的分泌升高,可能是其抗动脉粥样硬化的机制之一。而这一过程可能并不通过转化为雌雄激素而发挥,也许与其本身的生物学活性有关。     

The Influence of Specific Luminal Factors on the Colonic Epithelium: High-Dose Butyrate and Physical Changes Suppress Early Carcinogenic Events in Rats

INTRODUCTION Although luminal delivery of butyrate is one putative mechanism by which biology of the colonic epithelium might be influenced by changes in luminal contents, there is a paucity of supportive cause–effect evidence. This study aimed to directly establish whether distal colonic butyrate delivery is able to alter the response of the distal colonic epithelium to a carcinogen.METHODS Groups of male Sprague-Dawley rats with chronically intubated colons received infusions of 80 mM butyrate or 0.9 percent saline into distal colon two or five times daily. Three weeks after exposure to azoxymethane (15 mg/kg subcutaneously), the density of aberrant crypts was quantified in distal colon.RESULTS Infusions of 0.5 ml twice daily, whether containing saline or butyrate, decreased the number of aberrant crypt foci by 45 percent compared with rats receiving no infusions (P = 0.004, analysis of variance). Similar results were obtained when infusions were restricted to the postinitiation phase. When infusions were increased to 1 ml five times daily, saline infusions similarly suppressed aberrant crypt formation (38 percent), but butyrate infusions suppressed it to a greater degree (by 64 percent; P = 0.02 compared with saline infusion, t-test).CONCLUSIONS High levels of butyrate delivery to the distal colonic lumen alter the epithelial response to a carcinogen in otherwise healthy rats. This finding directly supports the notion that the effects of butyrate on cells in vitro do occur in vivo provided a sufficient dose is delivered. The effect of infusion of liquid per se on the epithelial response highlights the potential impact physical changes alone can have on the colonic epithelium.     

蚤休皂苷对氧化损伤的脐静脉内皮细胞间细胞粘附分子1和血管细胞粘附分子1表达的影响

目的研究中药蚤休皂苷对H2O2诱导的脐静脉内皮细胞ECV304损伤的保护作用及其机制。方法体外培养ECV304,建立氧化损伤细胞模型,然后分为五个实验处理组:正常对照组、氧化损伤组、高浓度蚤休皂苷组、中浓度蚤休皂苷组和低浓度蚤休皂苷组,采用四甲基偶氮唑盐比色法检测蚤休皂苷对H2O2诱导的内皮细胞氧化损伤的影响,逆转录聚合酶链反应检测细胞间细胞粘附分子1和血管细胞粘附分子1mRNA的表达水平,流式细胞术定量检测细胞间细胞粘附分子1和血管细胞粘附分子1的表达。结果损伤后细胞吸光度值低于正常对照组(P<0.01),药物预处理后吸光度值增加,高浓度蚤休皂苷组吸光度值与正常组相比差异无显著性;药物预处理氧化损伤后,细胞间细胞粘附分子1和血管细胞粘附分子1mRNA的表达水平与损伤组相比明显减弱(P<0.01);损伤组中与内参照的灰度值之比最大,与正常组相比差异显著(P<0.01);损伤组中表达细胞间细胞粘附分子1和血管细胞粘附分子1的阳性细胞数增多,与正常组相比差异显著(P<0.01);药物预处理氧化损伤后,阳性细胞数明显减少,且此效应呈剂量依赖性(P<0.01)。结论蚤休皂苷可以保护H2O2造成的人脐静脉内皮细胞的氧化损伤,是通过抑制内皮细胞粘附分子的表达从而抑制炎症性损伤,达到保护内皮细胞、抗动脉粥样硬化的目的。     

阿托伐他汀对同型半胱氨酸诱导的大鼠主动脉内皮细胞分泌前列腺素I2和单核细胞趋化蛋白1的影响

目的探讨不同浓度的阿托伐他汀对同型半胱氨酸损伤的大鼠主动脉内皮细胞分泌前列腺素I2、单核细胞趋化蛋白1的影响。方法体外培养大鼠动脉内皮细胞,待细胞生长至汇合状态时加入含浓度为50mmol/L同型半胱氨酸及不同浓度阿托伐他汀(5、15、30及50mmol/L)的培养液,孵育8h,检测细胞培养液中前列腺素I2、单核细胞趋化蛋白1水平。结果同型半胱氨酸明显损伤内皮细胞,使前列腺素I2水平明显降低,单核细胞趋化蛋白1水平显著升高。不同浓度的阿托伐他汀均可促进前列腺素I2分泌,抑制单核细胞趋化蛋白1分泌,并呈浓度依赖性(P<0.05)。结论阿托伐他汀可促进同型半胱氨酸损伤的大鼠动脉内皮细胞分泌前列腺素I2,抑制单核细胞趋化蛋白1的表达。     

The regulatory role of AT 1 receptor on activated HSCs in hepatic fibrogenesis:effects of RAS inhibitors on hepatic fibrosis induced by CCl(4)

AIM:To assess the effect of ACE inhibitor and Ang II type 1 (AT1) receptor antagonist in preventing hepatic fibrosis caused by CCl(4) administration in rats;to investigate whether or not there are expression of AT 1 receptors on hepatic stellate cells; and to observe the effect of Ang II on proliferation and ECM synthesis of cultured HSCs.METHODS:Studies were conducted in male Sprague-Dawley rats. Except for the hepatofibrotic model group and the control group, in three treated groups, either enalapril (5mg/kg), or losartan (10mg/kg), or enalapril + losartan were given to the fibrotic rats by daily gavage, and saline vehicle was given to model and normal control rats. After 6 weeks, liver fibrosis was assessed directly by hepatic morphometric analysis, which has been considered the gold standard for the quantification of fibrosis. The expressions of AT 1 receptors and (alpha-mooth muscle actin,alpha-SMA) in liver tissue or isolated hepatic stellate cells (HSCs) were detected by immunohistochemical techniques. The effect of Ang II on HSC proliferation was determined by MTT method. Effect of Ang II on collagen synthesis of HSCs was determined by (3)H-proline incorporation.RESULTS:Contrasted to the fibrosis in rats of the model group, groups of rats treated with either enalapril or losartan, or a combination of two drugs showed a limited expansion of the interstitium (4.23 plus minus 3.70 vs 11.22 plus minus 4.79, P<0.05), but no difference was observed among three treated groups (5.38 plus minus3.43, 4.96 plus minus 2.96, 4.23 plus minus 2.70, P>0.05). Expression of AT 1 receptors was found in fibrotic interstitium of fibrotic rats, whereas in normal control rats they were limited to vasculature only to a very slight degree. AT 1 receptors were also expressed on activated HSCs in the culture. At concentrations from 10(-9) to 10(-5)mol/L, Ang II stimulated HSC proliferation in culture in a dose dependent manner. Increasing Ang II concentrations produced corresponding increases in (3)H-proline incorporation. Differences among groups were significant.CONCLUSION:Angiotensin converting enzyme inhibitors and AT 1 blocker may slow the progression of hepatic fibrosis;activated HSCs express AT 1 receptors, and Ang II can stimulate the proliferation and collagen synthesis of HSCs in a dose-dependent manner; and activation of RAS may be related to hepatic fibrogenesis induced by CCl(4).     

On Growth and Morphology of TiO2 Nanotubes on Ti6Al4V by Anodic Oxidation in Ethylene Glycol Electrolyte: Influence of Microstructure and Anodization Parameters

Different studies demonstrated the possibility to produce TiO₂ nanotubes (TNTs) on Ti6Al4V alloy by electrochemical anodization. However, the anodizing behavior of α and β-phases in organic electrolytes is not yet clarified. This study reports on the anodizing behavior of the two phases in an ethylene glycol electrolyte using different applied potentials and anodizing times. Atomic force and scanning electron microscopies were used to highlight the anodic oxides differences in morphology. It was demonstrated that the initial compact oxide grew faster over the β-phase as the higher Al content of the α-phase caused its re-passivation, and the higher solubility of the V-rich oxide led to earlier pores formation over the β-phase. The trend was inverted once the pores formed over the compact oxide of the α-phase. The growth rate of the α-phase TNTs was higher than that of the β-phase ones, leading to the formation of long and well defined nanotubes with thin walls and a honeycomb tubular structure, while the ones grown over the β-phase were individual, shorter, and with thicker walls.