小儿MsPGN肾小管间质病变与激素疗效之间的关系

目的 探讨小儿系膜增殖性肾小球肾炎 (MsGPN)肾小管间质改变与激素疗效的关系。方法 根据患儿病理变化中有无肾小管间质改变分为肾小管间质病变组和肾小管间质无病变组 ,均予足量泼尼松治疗 ,比较两组激素疗效 ,进行 χ2 检验。结果 肾小管间质无病变组激素疗效明显优于有肾小管间质病变组 ,χ2 =12 .84 ,P <0 .0 1,差异有极显著性。结论 MsGPN中肾小管间质改变影响激素疗效 。

TNF_α在MsPGN中的作用研究进展

系膜增生性肾小球肾炎（MsPGN）在临床上发病率很高,我国约占原发性肾小球肾炎的30％。其发病机制尚不清楚。近十年来,随着细胞生物学和分子生物学研究进展,在肾脏病领域取得了重大突破,发现了一些细胞因子和生长因子在肾小球病变中起着关键性作用,TNF_α是其中重要细胞因子之一。笔者就TNF_α在MsPGN中的产生、作用及抗TNF_α治疗等进行综述。

MsPGN中活化NF-κBp65 mRNA、IL-1β mRNA、IL-4 mRNA的检测及其意义

目的:研究系膜增生性肾小球肾炎(MsPGN)肾组织中活化核因子-κBp65、IL-1β及IL-4基因表达的意义,探讨MsPGN的发病机制。方法:应用原位杂交技术分别检测正常对照组9例与病例组41例MsPGN肾组织中NF-κBp65mRNAI、L-1βmRNA及IL-4 mRNA水平,并分析3项检测指标之间的相互关系及其与MsPGN病变程度的关系。结果:(1)正常对照组中肾小球系膜区活化NF-κBp65mRNA、IL-1DmRNA阳性检出率分别为11.1%、33.3%,而IL-4 mRNA为0;病例组3项检测指标阳性率分别为70.7%、75.6%、61.1%。2组肾小球中3项检测指标阳性率差异有统计学意义(P<0.05)。(2)MsPGN肾小球组织中NF-κBp65mRNA活化与IL-1βmRNA之间呈显著正相关(r=0.383 6,P<0.05),IL-1βmRNA与IL-4mRNA之间亦呈显著正相关(r=0.477 1,P<0.01)。(3)活化NF-κBp65mRNAI、L-1βmRNA及IL-4mRNA阳性率均随着病变程度加重增高,但差异无统计学意义。(4)正常肾组织及MsPGN的肾小管中3项指标检测结果无一定规律性。结论:3项指标在MsPGN发病环节中共同起着作用。MsPGN对致病原的反应更接近于Th2反应。

青藤碱对MsPGN大鼠肾脏病理及ICAM-1表达的影响

为探讨青藤碱(Sinomenine,SIN)对实验性系膜增生性肾小球肾炎(MsPGN)的病理形态学改善及肾组织中细胞间粘附分子-1(ICAM-1)表达的影响,通过实验建立改良的慢性血清病性MsPGN动物模型,光镜观察肾小球以及肾小管-间质的病理改变情况,采用免疫组织化学法检测ICAM-1的表达并分别进行半定量分析。结果显示:光镜下,模型组与正常组相比,系膜基质指数显著升高(P<0.01),肾小球毛细血管直径明显缩小(P<0.01);青藤碱组与模型组相比,上述病理改变明显减轻,系膜基质指数显著下降(P<0.01),肾小球毛细血管直径明显改善(P<0.01)。肾组织中ICAM-1免疫组化结果显示青藤碱可明显下调ICAM-1的表达,肾组织ICAM-1的相对含量、积分光密度,均显著下降(P<0.01),青藤碱组与雷公藤多苷组相比,二者无统计学意义(P>0.05)。实验表明青藤碱能够有效减轻肾脏病理损害,抑制MsPGN大鼠肾组织ICAM-1的表达,延缓疾病进展。

PDGF,TGFβ,bFGF在人MsPGN中的表达及临床意义

目的 探讨细胞因子在人MsPGN疾病进展中的作用及其临床意义。方法 应用sABCf法对 2 8例MsPGN的肾活检组织进行了PDGF ,TGFβ ,bFGF检测。 结果 PDGF ,TGFβ ,bFGF主要表达于肾皮质区的肾小管内上皮 ,在轻度MsPGN的肾组织内表达高于中～重度MsPGN ,在硬化的肾小球周围萎缩的肾小管 ,伴有淋巴细胞浸润的区域 ,可见PDGF ,TGFβ ,bFGF阳性颗粒。 结论 PDGF ,TGFβ ,bFGF的过表达阶段 ,可刺激MC的增生 ,加重疾病的进展 ,此期给予上述细胞因子的抑制剂或拮抗剂进行治疗 ,可抑制或延缓MsPGN的进展 ,减少肾功能衰竭的发生。

MsPGN湿热型大鼠AQP-2表达及ADH变化的实验研究

目的研究系膜增生性肾炎(MsPGN)湿热型大鼠水通道蛋白-2(AQP-2)的表达及抗利尿激素(ADH)的变化及湿热蕴郁的机制,并探讨慢肾蛋白停对其的影响及作用机理。方法采用手术摘除一侧肾脏加腹腔多次注射牛血清白蛋白(BSA)与大肠杆菌内毒素(LPS)及皮下多次注射完全弗氏佐剂,复制MsPGN湿热模型,慢肾蛋白停予以防治性治疗,测定各组肾组织和血浆AQP-2及ADH。结果模型组大鼠血浆中AQP-2含量明显降低,肾组织AQP-2灰度值和血浆ADH含量明显升高,与正常对照组比较差异有统计意义(P<0.05)。而慢肾蛋白停组、肾炎四位片组能升高血浆AQP-2含量,降低肾组织AQP-2灰度值和血浆ADH含量,与模型组比较差异均有统计意义(P<0.05)。慢肾蛋白停组降低ADH含量较肾炎四位片组显著,两组比较差异有统计意义(P<0.05)。结论AQP-2与MsPGN湿热证表现出密切的相关性。慢肾蛋白停能增加血浆与肾组织AQP-2含量,降低血浆ADH水平。

Ⅲ、Ⅳ型胶原在人类MsPGN中的作用

作者将临床确诊为系膜增生性肾小球肾炎ＭｓＰＧＮ的病例分为轻、中、重三组，从每组中随机抽取１０例作为实验组１、２、３，取３例正常肾组织作为对照组。然后对所选取的３３例分别进行光镜图像分析，间接免疫荧光检查。结果显示：在Ｍａｓｓｏｎ三色染色的绿染部分分析结果中，中、重度ＭｓＰＧＮ与正常比较有显著性差异（ｐ＜０．０５）。ＰＡＳＭ黑染中，重度与正常比较有显著性差异（ｐ＜０．０５）。间接免疫荧光见：正常及空白对照组肾小球内未见Ⅲ型胶原，有少量Ⅳ型胶原分布于毛细血管基膜及系膜区。Ⅲ型胶原在中、重度ＭｓＰＧＮ中出现，Ⅳ型胶原随着病变进展明显增加。以上结果表明，在ＭｓＰＧＮ病变过程中Ⅲ、Ⅳ型胶原参与系膜基质扩增及肾小球硬化过程，图像分析可反应出ＭｓＰＧＮ的病变程度．

Changes of NF-kB,p53,Bcl-2 and caspase in apoptosis induced by JTE-522 in human gastric adenocarcinoma cell line AGS cells:role of reactive oxygen species

AIM: To identify whether JTE-522 can induce apoptosis inAGS cells and ROS also involved in the process, and toinvestigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process.METHODS: Cell culture, MTT, Electromicroscopy, agarosegel electrophoresis, lucigenin, Western blot andelectrophoretic mobility shift assay (EMSA) analysis wereemployed to investigate the effect of JTE-522 on cellproliferation and apoptosis in AGS cells and relatedmolecular mechanisms.RESULTS: JTE-522 inhibited the growth of AGS cells andinduced the apoptosis. Lucigenin assay showed the generationof ROS in cells under incubation with JTE-522. The inc eareasedROS generation might contribute to the induction of AGS cellsto apoptosis. EMSA and Westem blot revealed that NF-kBactivity was almost completely inhibited by preventing thedegradation of IkBα. Additionally, by using Western blot weconfirmed that the level of bcl-2 was decreased, whereas p53showed a great increase following JTE-522 treatment. Theirchanges were in a dose-dependent manner.CONCLUSION: These findings suggest that reactive oxygenspecies, NF-kB, p53, bcl-2 and caspase-3 may play animportant role in the induction of apoptosis in AGS cellsafter treatment with JTE-522.

Erucic acid from Isatis indigotica Fort. suppresses influenza A virus replication and inflammation in vitro and in vivo through modulation of NF-kB and p38 MAPK pathway

Isatis indigotica Fort.(Ban-Lan-Gen)is an herbal medicine prescribed for influenza treatment.However,its active components and mode of action remain mostly unknown.In the present study,erucic acid was isolated from Isatis indigotica Fort.,and subsequently its underlying mechanism against influenza A virus(IAV)infection was investigated in vitro and in vivo.Our results demonstrated that erucic acid exhibited broad-spectrum antiviral activity against IAV resulting from reduction of viral polymerase transcription activity.Erucic acid was found to exert inhibitory effects on IAV or viral(v)RNA-induced pro-inflam-matory mediators as well as interferons(IFNs).The molecular mechanism by which erucic acid with antiviral and anti-inflammatory properties was attributed to inactivation of NF-kB and p38 MAPK signaling.Furthermore,the NF-kB and p38 MAPK inhibitory effect of erucic acid led to diminishing the transcriptional activity of interferon-stimulated gene factor 3(ISGF-3),and thereby reducing IAV-triggered pro-inflammatory response amplification in IFN-β-sensitized cells.Additionally,IAV-or vRNA-triggered apoptosis of alveolar epithelial A549 cells was prevented by erucic acid.In vivo,erucic acid administration consistently displayed decreased lung viral load and viral antigens expression.Meanwhile,erucic acid markedly reduced CD8+cytotoxic T lymphocyte(CTL)recruitment,pro-apoptotic signaling,hyperactivity of multiple signaling pathways,and exacerbated immune inflammation in the lung,which resulted in decreased lung injury and mortality in mice with a mouse-adapted A/FM/1/47-MA(H1N1)strain infection.Our findings provided a mechanistic basis for the action of erucic acid against IAV-mediated inflammation and injury,suggesting that erucic acid may have a therapeutic potential in the treatment of influenza.

The clinical significance of CD97, NF-kB and COX-2 ingastric MALT lymphomas

Background and Objectives: Increased expression of the CD97, nuclear factor-kB (NF-kB) and cyclooxygenase-2 (COX-2) has been found to play an important role in development of many cancers, including gastric neoplasm. However, the expression and biological behavior of CD97, NF-kB and COX-2 in gastric MALT (mucosa-associated lymphoid tissue) lymphoma has not been well investigated. Methods: The expressions of CD97, COX-2 and NF-kB in 47 cases of gastric MALT lymphoma were detected immunohistochemically, and the relevance between their expressions and the biological behavior was analyzed retrospectively. Results: 1) The expressions of CD97, NF-kB and COX-2 were 87.2%, 36.2% and 48.9%, respectively;2) The difference of CD97 expression between depth of invasion limited in mucosa and submucosa and beyond muscularis propria was significant (100.0% vs. 71.4%, P < 0.01). Moreover, the expression of nuclear CD97 between stage IIE, III, IV and stage I patients showed significant difference (96.4% vs. 73.7%, P < 0.05);3) The expression of NF-kB was significantly correlated with tumor size, depth of invasion and stage;4) The expression of COX-2 was significantly correlated with Helicobacter pylori infection, clinical stage, depth of invasion and tumor size (P < 0.05). Conclusions: Expressions of CD97, NF-κB and COX-2 were correlated with tumor invasion and metastasis in gastric MALT lymphoma.

4＇, 6-Dihydroxy-4-methoxyisoaurone inhibits TNF-α-induced NF-KB activation and expressions of NF-KB-regulated target gene products

The nuclear factor-KB （NF-KB） transcription factors control many physiological processes including in- flammation, immunity, apoptosis, and angiogenesis. In our search for NF-KB inhibitors from natural resources, we identified 4＇,6-dihydroxy-4-methoxyisoaurone （ISOA） as an inhibitor of NF-KB activation from the seeds of Tricho- santhes kirilowii. However, the mechanism by which ISOA inhibits NF-KB activation is not fully understood. In the present study, we demonstrated the effect of ISOA on NF-KB activation in TNF-α-stimulated HeLa cells. This com- pound suppressed NF-KB activation through the inhibition of IKB kinase （IKK） activation. ISOA also has an influ- ence on upstream signaling of IKK through the inhibition of expression of adaptor proteins, TNF receptor-associated factor 2 （TRAF2） and receptor interacting protein 1 （RIP1）. Consequently, ISOA blocked the phosphorylation and degradation of the inhibitor of NF-KB alpha （IKBα） , and subsequent phosphorylation and nuclear translocation of p65. The suppression of NF-KB activation by ISOA led to the down-regulation of target genes involved in inflam- mation, proliferation, angiogenesis and invasion, as well as potentiation of TNF-α-induced apoptosis at least in part through activation of caspase-8. Taken together, this study extends our understanding on the mechanisms underly- ing the anti-inflammatory and anti-cancer activities of ISOA. Our findings provide new insight into the molecular mechanisms and a potential application of ISOA for inflammatory diseases as well as certain cancers associated with abnormal NF-KB activation.

Magnesium lithospermate B inhibits lipopolysaccharide-induced endothelial activation through NF-KB pathway

Aim Magnesium lithospermate B （MLB） is the most abundant hydrophilic active component of Salvia rniltiorrhiza Radix, a traditional Chinese herbal medicine mainly used to treat cardiovascular diseases. Studies have shown that endothelial activation contributes to the pathophysiology of cardiovascular diseases such as atherosclero- sis, diabetic vasculopathy, heart failure and hypertension. In the present study, the effects of MLB on endothelial activation were investigated. Lipopolysaccharide （LPS） 1 mg L^-1 was employed to induce endothelial activation, which was determined by relative gene expression and endothelial adhesion assay. Results showed that pretreatment with MLB attenuated LPS-induced ICAM1, VCAM1 and TNF-α upregulation in human dermal microvascular endo- thelial cells （HMEC-1） in dose-dependent manner, which contributed to the reduction of THP-1 adhesion to HMEC-1. Furthermore, it was revealed that 100 μmol · L^-1 MLB significantly decreased the nuclear translocation of NF-KB p65, a critical transcription factor in LPS-indueed inflammatory response, through the inhibition of IKBμ degradation. Besides, the transcriptional activity of NF-KB p65 was also inhibited by the pretreatment of MLB. Mo- reover, MLB pretreatment considerably inhibited LPS-induced p38 phosphorylation, which at least partly contribu- ted to the reduction of ICAM1 expression. In conclusion, these findings suggest that MLB inhibits LPS-induced nu- clear translocation and transcripitional activity of NF-KB, thus attenuates the increased expression of adhesion mole- cules and inflammatory factors, protects endothelial cells from LPS-induced activation.

Effects of Tripterygium wilfordii combined with viaminate capsules on psoriasis patients' immune indexes, endothelium, inflammatory reaction, sICAM-1 and NF-kB

Objective: To explore the effects of Tripterygium wilfordii combined with viaminate on psoriasis patients' immune indexes, endothelium, inflammatory reaction, sICAM-1 and NF-kB. Methods: A total of 112 patients with psoriasis admitted in our hospital from September 2015 to November 2017 were randomly divided into control group (n=56) and observation group (n=56). The control group was treated only by Viaminate Capsules, and the observation group was treated with Tripterygium wilfordii tablet on the basis of the control group, the immune function, endothelial, inflammatory response, soluble intercellular adhesion molecules-1 (sICAM-1) and nuclear transcription factor-kB (NF-kB) expression levels were compared before and after treatment in the two groups. Results: Before treatment, CD4+, CD8+, CD4+/CD8+, vascular endothelial growth factor (VEGF), nitric oxide (NO), endothelin-1 (ET-1), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), NF-kB, and sICAM-1 in two groups were no significant difference. After treatment, CD4+and CD4+/CD8+in both groups were significantly increased, while CD8+was significantly lower than before treatment, the CD4+and CD4+/CD8+in the observation group were significantly higher than those in the control group, and CD8+was obviously lower than that of the control group;The VEGF, NO and ET-1 in both groups were dramatically lower than those before treatment, and the VEGF, NO and ET-1 in the observation group were significantly lower than those in the control group;The TNF-α and IFN-γ in two groups were significantly lower than before treatment, and TNF-α and IFN-γ in the observation group were remarkably lower than those in the control group;The NF-kB and sICAM-1 in two groups were obviously decreased than those before treatment, and the NF-kB and sICAM-1 in the observation group were significantly lower than those in the control group. Conclusion: Tripterygium wilfordii combined with viaminate capsules in the treatment of psoriasis patients, can effectively correct their immune dysfunction, improve endothelial function, reduce inflammatory response and inhibit the expression of NF-kB and sICAM-1 expression.

鱼酱排毒合剂对急性鼻窦炎大鼠NF-kB通路的影响

目的研究鱼酱排毒合剂对急性鼻窦炎大鼠核转录因子-kB(NF-kB)通路相关蛋白表达的影响。方法采用单侧鼻腔接种金黄色葡萄球菌建立大鼠急性鼻窦炎模型,根据急性鼻窦炎评分表评估造模结果。将成模大鼠分为正常组、模型组、鱼酱组(予鱼酱排毒合剂)和阿莫西林组(予阿莫西林克拉维酸分散片),各组给予相应药物治疗7d。治疗结束后测定各组大鼠鼻腔分泌物的pH值;HE染色观察鼻黏膜组织病理学改变;ELISA检测鼻腔灌洗液及鼻黏膜上清液中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)水平;Westernblotting检测NF-kB信号通路相关蛋白表达水平。结果急性鼻窦炎大鼠炎症模型成功建立。与模型组相比,鱼酱组和阿莫西林组大鼠鼻腔分泌pH值显著降低(P<0.01),鼻黏膜病理损伤明显改善,鼻腔灌洗液和鼻黏膜组织上清液中TNF-α、IL-1β、IL-6水平明显降低(P<0.01),NF-kB相关蛋白表达水平显著下降(P<0.01)。结论鱼酱排毒合剂可通过调节急性鼻窦炎大鼠NF-kB相关信号蛋白的表达,从而改善大鼠急性鼻窦炎症状。

Transcriptomic analysis identifies the neuropeptide cortistatin (CORT) as an inhibitor of temozolomide (TMZ) resistance by suppressing the NF-kB-MGMT signaling axis in human glioma

Glioma is a common tumor originating in the brain that has a high mortality rate.Temozolomide(TMZ)is the first-line treatment for high-grade gliomas.However,a large pro-portion of gliomas are resistant to TMZ,posing a great challenge to their treatment.In the study,the specific functions and mechanism(s)by which cortistatin(CORT)regulates TMZ resis-tance and glioma progression were evaluated.The decreased expression of CoRT was detected in glioma tissues,and highly expressed CORT was associated with a better survival rate in pa-tients with glioma.CORT overexpression notably decreased the capacity of glioma cells to pro-liferate and migrate in vitro and to form tumors in vivo.CORT overexpression also markedly suppressed the viability and enhanced the apoptosis of TMZ-resistant U251 cells by regulating MGMT,p21,and Puma expression.Importantly,CORT overexpression reduced the resistance of gliomas to TMZ in vivo.CORT expression Was negatively correlated with MGMT expression in both glioma tissues and cells,and it was found that CORT inhibited NF-kB pathway activation in glioma cells,thereby inhibiting MGMT expression.In conclusion,CORT regulates glioma cell growth,migration,apoptosis,and TMZ resistance by weakening the activity of NF-kB/p65 and thereby regulating MGMT expression.The CORT/NF-kB/MGMT axis might be regarded as a molecular mechanism contributing to the resistance of glioma to TMZ.Our data also suggest that CORT regulates the viability and metastatic potential of glioma cells,independent of its effects on TMZ resistance,providing evidence of novel therapeutic targets for glioma that should be evaluated infurther studies.

蛇床子素通过NF-kB信号通路调控退变髓核细胞的细胞外基质表达、炎症反应及凋亡

目的 研究蛇床子素对退变髓核细胞的细胞外基质表达、炎症反应和凋亡的作用及其潜在机制。方法 采用氧糖剥夺(Oxygen Glucose Deprivation, OGD)培养建立退变髓核细胞模型,将细胞分为:对照组(正常培养)、OGD组(OGD培养)、蛇床子素组(OGD培养+蛇床子素处理)、PDTC组(OGD培养+NF-κB通路抑制剂PDTC处理)和蛇床子素+PDTC组(OGD培养+蛇床子素+PDTC处理)。采用Western blot检测细胞中Ⅱ型胶原(Collagen typeⅡ,Col2al)、聚集蛋白聚糖(Aggrecan)、P65和p-P65蛋白表达,ELISA法检测细胞培养液中炎性因子血清白细胞介素-1β(interleukin-1 β,IL-1β),白细胞介素-6(interleukin-6,IL-6)和肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)的水平,流式细胞仪检测细胞凋亡率。结果 与对照组比较,OGD组细胞中Col2al、Aggrecan蛋白相对表达水平明显降低,细胞培养液中IL-1β、IL-6和TNF-α水平升高,细胞凋亡率明显升高,细胞中p-P65蛋白表达明显升高;与OGD组比较,蛇床子素组和PDTC组细胞中Col2al、Aggrecan蛋白相对表达水平明显升高,细胞培养液中IL-1β、IL-6和TNF-α水平降低,细胞凋亡率明显降低,细胞中p-P65蛋白表达明显降低,而蛇床子素+PDTC组上述指标改变最为明显。结论 蛇床子素可能通过抑制核因子激活的B细胞的κ轻链增强(nuclear factorκB,NF-κB)信号通路的活性,促进退变髓核细胞的细胞外基质合成、抑制退变髓核细胞的炎症反应和凋亡。

川芎嗪通过调控Txnip/TRX/NF-kB通路对急性肺损伤小鼠的保护作用研究

目的探索川芎嗪对脂多糖(LPS)诱导的急性肺损伤(ALI)小鼠的保护作用,并探寻其可能的作用机制。方法选取50只健康BABL/c小鼠,随机分为对照组、模型组、地塞米松组(2mg/kg)川芎嗪低剂量组(20mg/kg)和川芎嗪高剂量组(40mg/kg)。对照组和模型组给予生理盐水,地塞米松组(2mg/kg)、川芎嗪组(20、40mg/kg)灌胃给予相应药物。给药1h后,除对照组外,其余各组小鼠气管滴注20μgLPS。测定小鼠肺湿/干质量比,观察肺组织病理学变化,相应试剂盒检测肺组织超氧化物歧化酶(SOD)水平和丙二醛(MDA)含量,ELISA法检测白细胞介素-1β(1L-1β)和肿瘤坏死因子-α(TNF-α)表达,Westernblotting检测Txnip、TRX和p-NF-kB p65蛋白表达。结果川芎嗪可显著缓解LPS诱导的ALI小鼠的肺水肿程度(P<0.01);显著上调SOD活力,下调MDA含量(P<0.05);有效降低小鼠肺组织炎性细胞因子表达水平(P<0.05);降低Txnip、p-NF-kBp65的表达,上调TRX的表达(P<0.05)。结论川芎嗪可能通过Txnip/TRX/NF-kB信号通路缓解LPS诱导的ALI。

山药山楂茶对糖尿病阳痿模型大鼠阴茎NF-KB的影响

目的 观察山药山楂茶对糖尿病性阳痿模型大鼠阴茎核转录因子NF-kB(nuclear factor-kappa B)的影响。方法 取SPF(Specefic pathogen Free)级5月龄雄性GK(Goto Kakizaki)大鼠45只,随机分为空白组、模型组、治疗组,另设15只Wistar大鼠为正常组;予以一氧化氮合成酶(eNOS)抑制剂L-NAME造模,高脂饲料喂养,药茶灌胃4w。观察大鼠一般情况,阴茎勃起次数及勃起率,采用酶联免疫吸附法(ELISA)检测各组大鼠血清睾酮水平、Western Blot法检测阴茎海绵体NF-kB蛋白水平。结果 模型组与正常组及空白组相比,模型组勃起率和勃起次数明显低于正常组(P<0.01)和空白组(P<0.05);治疗组勃起率和勃起次数明显高于模型组(P<0.01);治疗组与正常组相比,两组勃起率和勃起次数无明显差异(P>0.05);模型组血清睾酮水平低于治疗组(P<0.05);模型组阴茎NF-kB蛋白水平明显高于治疗组(P<0.01)。结论 山药山楂茶可以改善糖尿病性阳痿大鼠勃起功能,可以调节糖尿病性阳痿大鼠阴茎海绵体(NF-kB)蛋白水平。