[Protective effect of Ligustri Lucidi Ait Polysaccharide against lipopolysaccharide-induced inflammatory injury of Sertoli cells in rats].

OBJECTIVE: To explore the effect of Ligustri Lucidi Ait Polysaccharide (LLP) on lipopolysaccharide (LPS)-induced inflammatory injury of Sertoli cells. METHODS: Rat Sertoli cells were isolated and cultured in vitro and then divided into five groups, blank control, LPS, LPS + low-dose LLP, LPS + medium-dose LLP, and LPS + high-dose LLP. After 48 hours of treatment, the proliferation of the cells was detected by CCK-8, their apoptosis determined by FMC, and the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) in the supernatant of the cell culture medium measured by ultraviolet spectrophotometry. The contents of IL-1α, IL-6 and TGF-ß in the culture medium were detected by ELISA before and after removal of LPS. RESULTS: The proliferation of the cells showed statistically significant differences among different groups (F = 153.93, P < 0.01), markedly reduced in the LPS group as compared with the blank control (P < 0.01), but remarkably increased in the high- and medium-dose LLP groups in comparison with the LPS group (both P < 0.01), and so did the apoptosis of the cells (F = 64.06, P < 0.01), significantly increased in the LPS group as compared with the blank control (P < 0.05), but markedly decreased in the high- and medium-dose LLP groups in comparison with the LPS group (both P < 0.01). Statistically significant differences were also observed among different groups in the levels of SOD (F = 56.07, P < 0.01), CAT (F = 41.57, P < 0.01), GSH-Px activity (F = 238.46, P < 0.01), and MDA (F = 285.31, P < 0.01), with decreased SOD, CAT and GSH-Px activity (P < 0.01) and increased MDA (P < 0.01) in the LPS group as compared with the control, but elevated SOD and CAT in the high- and medium-dose LLP groups and increased GSH-Px activity and decreased MDA concentration in all the three LLP groups in comparison with the LPS group (P < 0.01). Before the removal of LPS, the contents of IL-1α, IL-6 and TGF-ß in the culture medium were markedly higher in the LPS than in the control group (all P < 0.01), that of IL-1α was increased significantly in the high- and medium-dose LLP groups (P < 0.01 and P < 0.05) while those of IL-6 and TGF-ß showed no statistically significant differences in the three LPS groups as compared with the LLP group (P > 0.05). After the removal of LPS, the contents of IL-1α and IL-6 were remarkably reduced (t = 25.26 and 61.43, P < 0.01) and that of TGF-ß increased (t = －18.16, P < 0.01), even more significantly in the LLP+LPS groups (P < 0.01). CONCLUSIONS: Ligustri Lucidi Ait Polysaccharide plays a protective role in LPS-induced inflammatory injury of Sertoli cells by reducing cell apoptosis and regulating the contents of IL-1α, IL-6 and TGF-ß from Sertoli cells in inflammation.

The Molecular Profile of Soil Microbial Communities Inhabiting a Cambrian Host Rock.

The process of soil genesis unfolds as pioneering microbial communities colonize mineral substrates, enriching them with biomolecules released from bedrock. The resultant intricate surface units emerge from a complex interplay among microbiota and plant communities. Under these conditions, host rocks undergo initial weathering through microbial activity, rendering them far from pristine and challenging the quest for biomarkers in ancient sedimentary rocks. In addressing this challenge, a comprehensive analysis utilizing Gas Chromatography Mass Spectrometry (GC-MS) and Time-of-Flight Secondary Ion Mass Spectrometry (ToF-SIMS) was conducted on a 520-Ma-old Cambrian rock. This investigation revealed a diverse molecular assemblage with comprising alkanols, sterols, fatty acids, glycerolipids, wax esters, and nitrogen-bearing compounds. Notably, elevated levels of bacterial C16, C18 and C14 fatty acids, iso and anteiso methyl-branched fatty acids, as well as fungal sterols, long-chained fatty acids, and alcohols, consistently align with a consortium of bacteria and fungi accessing complex organic matter within a soil-type ecosystem. The prominence of bacterial and fungal lipids alongside maturity indicators denotes derivation from heterotrophic activity rather than ancient preservation or marine sources. Moreover, the identification of long-chain (>C22) n-alkanols, even-carbon-numbered long chain (>C20) fatty acids, and campesterol, as well as stigmastanol, provides confirmation of plant residue inputs. Furthermore, findings highlight the ability of contemporary soil microbiota to inhabit rocky substrates actively, requiring strict contamination controls when evaluating ancient molecular biosignatures or extraterrestrial materials collected.

Clinical outcomes and risk factors of non-curative endoscopic submucosal dissection for early gastric cancer: a retrospective multicenter study in Zhejiang, China.

Background: Endoscopic submucosal dissection (ESD) for early gastric cancer (EGC) does not always lead to curative resection. Risk factors of lymph node metastasis (LNM)/local cancer residue after non-curative ESD for EGC have not been fully elucidated. We therefore aimed to clarify them and evaluate whether the "eCura system" is reliable for the risk stratification of LNM after non-curative ESD. Methods: We conducted a multicenter retrospective study at seven institutions in Zhejiang, China, on 128 patients who underwent non-curative ESD for EGC. We divided the patients into two groups according to their therapeutic regimen after non-curative ESD. We analyzed the risk factors for LNM, local cancer residue, cancer recurrence, and cancer-specific mortality. Furthermore, we compared the outcomes in each risk category after applying the "eCura system". Results: Among 68 patients undergoing additional surgery, LNM was found in three (4.41%) patients, while local cancer residue was found in eight (11.76%) patients. Multivariate analysis showed that upper third location and deep submucosal invasion were independent risk factors of LNM and local cancer residue. Among 60 patients who underwent simple follow-up, local cancer recurrence was found in four (6.67%) patients and cancer-specific mortality was found in one (1.67%) patient. There were no independent risk factors of cancer recurrence and cancer-specific mortality in our study. During the follow-up period, 5-year overall survival (OS) and disease-free survival (DFS) were 93.8% and 88.9%, respectively. Additionally, LNM and cancer recurrence were significantly associated with the eCura scoring system (p = 0.044 and p = 0.017, respectively), while local cancer residue and cancer-specific mortality were not (p = 0.478 and p = 0.131, respectively). Conclusion: Clinicians should be aware of the risk factors for the prognosis of patients with non-curative ESD to determine subsequent treatment. Through the application of the "eCura system", additional surgery should be performed in patients with intermediate/high risk of LNM.

T140 Inhibits Apoptosis and Promotes Proliferation and Matrix Formation Through the SDF-1/CXC Receptor-4 Signaling Pathway in Endplate Chondrocytes of the Rat Intervertebral Discs.

BACKGROUND: Cartilaginous endplate (CEP), a thin layer of hyaline cartilage located between the vertebral endplate and nucleus pulposus, transports the nutrient into the disc. The objective of this study was to evaluate the influence of T140 (polyphemusin II-derived peptide) on the CEP cell growth, apoptosis, and the matrix formation via the stromal cell-derived factor-1 (SDF-1)/cysteine X cysteine (CXC) receptor-4 (CXCR4) signaling pathway. METHODS: Sprague-Dawley rats were euthanized by cervical dislocation and dissected for the isolation and the appraisal of CEP cells that were extracted from the endplate in rat intervertebral discs and were then added with different concentrations of reagents (SDF-1 and T140). The effect of T140 on CEP cell proliferation and apoptosis were analyzed. The messenger RNA (mRNA) and protein expressions of CXCR4, prominin-1, proteoglycans, type II collagen, B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein were analyzed by reverse transcription quantitative polymerase chain reaction and Western blot analysis. RESULTS: T140 promoted the proliferation of CEP cells and inhibited the apoptosis of CEP cells. Additionally, T140 suppressed the mRNA and protein expression of CXCR4, prominin-1, and Bcl-2 associated X protein, and increased the mRNA and protein expression of proteoglycans, type II collagen, and Bcl-2. CONCLUSIONS: T140 promotes the proliferation and matrix formation and inhibits the apoptosis of CEP cells by blocking the SDF-1/CXCR4 signaling pathway in vitro, which provides a certain therapeutic effect on the degeneration of intervertebral discs.

Phosphoinositide 3-kinase/Akt pathway plays an important role in chemoresistance of gastric cancer cells against etoposide and doxorubicin induced cell death.

The major obstacle to successful treatment of gastric cancer is chemotherapy resistance. Our study was designed to investigate the role of phosphoinositide 3-kinase (PI3K)/Akt pathway in the development of chemoresistance in gastric cancer. In the present study, elevated Akt expression and Akt phosphorylation (Ser 473), as well as decreased PTEN expression were observed in 28 cases of gastric cancer tissues. Etoposide and doxorubicin stimulated Akt and PI3K activities in 2 gastric cancer cell lines (BGC-823 and SGC-7901), and the activities were concentration and time-dependent. Up-regulation of PTEN expression in BGC-823 cells by PEAK8-PTEN transient transfection obviously decreased the basal and anticancer drugs induced Akt activities, then sensitized BGC-823 cells to etoposide and doxorubicin. Pretreatment of BGC-823 and SGC-7901 cells with wortmannin, a PI3K inhibitor, attenuated cells's resistance to etoposide and doxorubicin. In addition, pretreatment of wortmannin blocked etoposide and doxorubicin induced IkappaB-alpha degradation, NFkappaB activation, phosphorylation of Akt, MDM-2 and forkhead transcription factors. Wortmannin pretreatment also promoted the accumulation of p27/Kip, but inhibited the Mcl-1 expression. Furthermore, wortmannin promoted etoposide and doxorubicin induced caspase-3, caspase-9 activation and poly ADP-ribose polymerase cleavage. Taken together, the observations indicate the PI3K/Akt pathway plays an important role in the chemoresistance of gastric cancer cells. A new strategy for combined chemotherapy of gastric cancer should be designed to more specifically block PI3K/Akt pathway and then decrease the amount of resistant cells.

Two-tube method for treatment of spontaneous esophageal rupture and concomitant mediastinal infection.

Objective Spontaneous esophageal rupture (SER) is a rare but life-threatening condition with high mortality. The prognosis of patients with SER treated with surgical intervention or the traditional "three-tube" method is controversial. Thus, the aim of this study was to evaluate the clinical efficacy, feasibility, and safety of a new "two-tube" method involving a trans-fistula drainage tube and a three-lumen jejunal feeding tube for the treatment of SER without concomitant pleural rupture. Methods From January 2007 to June 2016, patients with SER and managed with the "two-tube" method or other methods were retrospectively analyzed. Data collected included initial presentation, procedure time, duration of treatment, numbers of patients with eventual healing of leaks, and complications. Results The average procedure time for the "two-tube" method was 22.1 ± 5.5 minutes. In comparison with the control method, the "two-tube" method had a similar diagnosis time (3.6 ± 1.4 vs. 3.4 ± 1.4 days) but a significantly higher successful closure rate (94.4% vs. 63.6%) and shorter treatment time (38.2 ± 5.6 vs. 53.6 ± 16.9 days). No complications associated with performance of the "two-tube" method occurred. Conclusion The "two-tube" method is an effective and safe approach for patients with SER.

Expression and significance of nuclear factor kappaB p65 in colon tissues of rats with TNBS-induced colitis.

AIM: To investigate the role of NF-kappaB in the pathogenesis of TNBS-induced colitis in rats. METHODS: Thirty-two healthy adult Sprague-Dawley (SD) rats were randomly divided into four groups of eight each: normal, NS, model I, model II groups in our study. Rat colitis model was established through 2-,4-,6-trinitrobenzene sulfonic acid (TNBS) enema. At the end of four weeks, the macroscopical and histological changes of the colon were examined and mucosa myeloperoxidase (MPO) activities assayed. NF-kappaB p65 expression was determined by Western blot assessment in cytoplasmic and nuclear extracts of colon tissue, and the expressions of TNF-alpha and ICAM-1 protein in colon tissue were examined by immunohistochemistry. The relativities between expression of NF-kappaB p65 and other parameters were analyzed. RESULTS: TNBS enema resulted in pronounced pathological changes of colonic mucosa in model II group (macroscopic and histological injury indices 6.25+/-1.39 and 6.24+/-1.04, respectively), which were in accordance with the significantly elevated MPO activity (1.69+/-0.11). And the nuclear level of NF-kappaB and expression of TNF-alpha, ICAM-1 in rats of model II group were higher than that of normal control (9.7+/-1.96 vs 1.7+/-0.15, 84.09+/-14.52 vs 16.03+/-6.21, 77.69+/-8.09 vs 13.41+/-4.91 P<0.01), Linear correlation analysis revealed that there were strong correlations between the nuclear level of NF-kappaB and the tissue positive expression of TNF-alpha and ICAM-1, MPO activities, macroscopical and histological indices in TNBS-induced colitis, respectively (r = 0.8235, 0.8780, 0.8572, 0.9152, 0.8247; P<0.05). CONCLUSION: NF-kappaB plays a pivotal role in the pathogenesis of ulcerative colitis, which might account for the up-regulation the expression of TNF-alpha and ICAM-1.

Effects of garlicin on apoptosis in rat model of colitis.

AIM: To investigate the effects of garlicin on apoptosis and expression of bcl-2 and bax in lymphocytes in rat model of ulcerative colitis (UC). METHODS: Healthy adult Sprague-Dawley rats of both sexes, weighing 180+/-30 g, were employed in the present study. The rat model of UC was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) enema. The experimental animals were randomly divided into garlicin treatment group (including high and low concentration), model control group, and normal control group. Rats in garlicin treatment group and model control group received intracolic garlicin daily at doses of 10.0 and 30.0 mg/kg and equal amount of saline respectively 24 h after colitis model was induced by alcohol and TNBS co-enema. Rats in normal control group received neither alcohol nor only TNBS but only saline enema in this study. On the 28th d of the experiment, rats were executed, the expression of bcl-2 and bax protein was determined immunohistochemically and the apoptotic cells were detected by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate fluorescence nick end labeling (TUNEL) method. At the same time, the rat colon mucosal damage index (CMDI) was calculated. RESULTS: In garlicin treatment group, the positive expression of bcl-2 in lymphocytes decreased and the number of apoptotic cells was more than that in model control group, CMDI was lower than that in model control group. The positive expression of bax in lymphocytes had no significant difference. CONCLUSION: Garlicin can protect colonic mucosa against damage in rat model of UC induced by TNBS enema.

[Ecological compensation based on farmers' willingness: A case study of Jingsan County in Hubei Province, China].

Farmland protection is a pressing issue in China' s major agricultural regions because of the strategic importance of these regions for national food security. This study quantified the appropriate ecological compensation criteria for farmland protection by way of estimating farmers' opportunity cost and willingness to adopt environment-friendly farming practices. Based on survey data collected from Jingsan County, Hubei Province, a Tobit model was constructed to identify factors affecting farmers' willingness to accept (WTA). The result showed that with appropriate economic compensation for farmland protection, 77.1% and 64.7% of the surveyed households were willing to reduce usage of fertilizers and pesticides. When the reduced rates of fertilizer and pesticide increased from <10% to >50%, farmers' opportunity costs of production respectively increased from 1198 and 5850 yuan to 9698 and 9750 yuan per hectare per year, and their WTA increased from 4750 and 7313 yuan to 9781 and 12393 yuan per hectare per year. Farmers' opportunity cost and WTA in reducing pesticide inputs were larger than those in reducing the same rate of fertilizer inputs, and in each case farmers' WTA was greater than their opportunity cost. A farm' s distance from township, farmers' knowledge about the ecology of farmland, and their expectation to improve the ecological environment of farmland had positive, significant effect on the farmers' WTA to reducing fertilization, while farmers' education level and the overall economic condition of the village had significantly negative effect. The proportion of agriculture income, farmers' knowledge about the ecology of farmland, and their expectation to improve the ecological environment of farmland had positive, significant effect on the farmers' WTA to reducing pesticide, while household' cash income and the overall economic condition of the village had significantly negative effect.

Nuclear factor-kappaB p65 (RelA) transcription factor is constitutively activated in human colorectal carcinoma tissue.

AIM: Activation of transcription factor nuclear factor-kappaB (NF-kappaB) has been shown to play a role in cell proliferation, apoptosis, cytokine production, and oncogenesis. The purpose of this study was to determine whether NF-kappaB was constitutively activated in human colorectal tumor tissues and, if so, to determine the role of NF-kappaB in colorectal tumorigenesis, and furthermore, to determine the association of RelA expression with tumor cell apoptosis and the expression of Bcl-2 and Bcl-x(L). METHODS: Paraffin sections of normal epithelial, adenomatous and adenocarcinoma tissues were analysed immunohistochemically for expression of RelA, Bcl-2 and Bcl-x(L) proteins. Electrophoretic mobility shift assay (EMSA) was used to confirm the increased nuclear translocation of RelA in colorectal tumor tissues. The mRNA expressions of Bcl-2 and Bcl-x(L) were determined by reverse transcription polymerase chain reaction (RT-PCR) analysis. Apoptotic cells were detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate fluorescence nick end labeling (TUNEL) method. RESULTS: The activity of NF-kappaB was significantly higher in adenocarcinoma tissue in comparison with that in adenomatous and normal epithelial tissues. The apoptotic index (AI) significantly decreased in the transition from adenoma to adenocarcinoma. Meanwhile, the expressions of Bcl-2 and Bcl-x(L) protein and their mRNAs were significantly higher in adenocarcinoma tissues than that in adenomatous and normal epithelial tissues. CONCLUSION: NF-kappaB may inhibit apoptosis via enhancing the expression of the apoptosis genes Bcl-2 and Bcl-x(L). And the increased expression of RelA/nuclear factor-kappaB plays an important role in the pathogenesis of colorectal carcinoma.

Nuclear factor-kappa B regulates cyclooxygenase-2 expression and cell proliferation in human colorectal carcinoma tissue.

OBJECTIVE: Activation of transcription factor nuclear factor-kappa B (NF-kappa B) has been shown to play a role in cell proliferation, apoptosis, cytokine production, and oncogenesis. The purpose of this study was to determine whether NF-kappa B is constitutively activated in human colorectal tumor tissues and, if so, to determine the role of NF-kappa B in colorectal tumorigenesis, furthermore, to determine the association of RelA expression with the expression of cyclooxygenase-2 (COX-2) and tumor cell proliferation. METHODS: Paraffin sections of the normal epithelial, adenomatous and adenocarcinoma tissue were analysed immunohistochemically for RelA, COX-2, Ki-67 protein expression. EMSA (electrophoretic mobility shift assay) was used to confirm the increased nuclear translocation of RelA in colorectal tumor tissues. The expression of COX-2 mRNA was determined by RT-PCR (reverse transcription polymerase chain reaction) analysis. RESULTS: Activation of NF-kappa B was significantly higher in adenocarcinoma tissue in comparison to that in adenomatous and normal epithelial tissue. The colon tumor cell proliferation, mRNA expression and protein level of COX-2 were significantly increased in the transition from normal to tumor tissue. CONCLUSION: Our results suggest that NF-kappa B may promote proliferation via enhancing the expression of COX-2, and the increased expression of RelA/nuclear factor-kappa B plays an important role in the pathogenesis of colorectal carcinoma.

Curcumin reverses chemoresistance of human gastric cancer cells by downregulating the NF-κB transcription factor.

Gastric cancer remains one of the major health problems worldwide. Chemotherapy is an important therapeutic modality for gastric cancer, but the success rate of this treatment is limited because of chemoresistance. The ubiquitously expressed transcription factor NF-κB has been suggested to be associated with chemoresistance of gastric cancer. Agents that can either enhance the effects of chemotherapeutics or overcome chemoresistance to chemotherapeutics are needed for the treatment of gastric cancer. Curcumin, a component of turmeric, is one such agent that has been shown to suppress NF-κB and increase the efficacy of chemotherapy. In this study, we investigated whether curcumin can reverse chemoresistance by downregulating NF-κB in human gastric cancer cells. SGC-7901 human gastric cancer cells was treated with chemotherapeutics (etoposide and doxorubicin) or by combined application of curcumin and chemotherapeutics. The viability of SGC-7901 cells was measured by MTT assay. Apoptosis of SGC-7901 cells was detected using the TUNEL and Annexin V/PI methods. The protein levels of NF-κB were analyzed by immunocytochemical staining. EMSA was used to confirm the increased nuclear translocation of RelA. The protein levels of p-IκBα, Bcl-2 and Bcl-xL were analyzed by Western blotting. The chemotherapeutics (etoposide and doxorubicin) suppressed the growth of SGC-7901 cells, in a time-dose-dependent manner. Use of curcumin in addition to these agents can suppress cell growth further (inhibitory rate: doxorubicin vs. doxorubicin + curcumin, 33% vs. 45%, p<0.05; etoposide vs. etoposide + curcumin, 35% vs. 48%, p<0.05). Furthermore, chemotherapeutics induced apoptosis of SGC-7901 cells and activated NF-κB. The combination of curcumin and chemotherapeutics induced apoptosis of SGC-7901 cells further, attenuated the activation of NF-κB, and reduced expression of the NF-κB-regulated anti-apoptotic gene products Bcl-2 and Bcl-xL. Curcumin potentiates the antitumor effects of chemotherapeutics in gastric cancer by suppressing NF-κB and NF-κB-regulated anti-apoptotic genes.

Akt associates with nuclear factor kappaB and plays an important role in chemoresistance of gastric cancer cells.

The ubiquitously expressed serine-threonine kinase Akt and the transcription factor NF-kappaB both are involved in cell proliferation and apoptosis. Furthermore, the activation of Akt or NF-kappaB has been suggested to associate with chemo-resistance of human tumors. The exact mechanism and interreaction of Akt and NF-kappaB pathway on chemoresistance in gastric cancer is still unknown. We explored the function of Akt and NF-kappaB pathway on chemoresistance in human gastric cancer cells. MTT method was used to analyze the influence of chemotherapeutics and the combined use of wortmannin or MG-132 on the growth of SGC-7901 cells. Apoptosis of SGC-7901 was detected by TUNEL and Annexin V/PI methods. The protein level of NF-kappaB was analyzed by immunocytochemical staining. EMSA was used to confirm the increased nuclear translocation of RelA. The protein level of p-Akt and p-IkappaBalpha were analyzed by Western blotting. Etoposide and doxorubicin suppressed the growth of SGC-7901 time and dose-dependently. Combined use of wortmannin or MG-132 can suppress growth further. Chemotherapeutics induced apoptosis of SGC-7901 and activated Akt and NF-kappaB, combined use of wortmannin or MG-132 induced apoptosis further and attenuated the activation of NF-kappaB. The combined use of wortmannin attenuated the activation of Akt, but combined use of MG-132 did not attenuate the activation of Akt. The activation of NF-kappaB is a branch mechanism of Akt anti-apoptosis effects. The chemotherapeutics induced apoptosis and induced the activation of Akt and NF-kappaB in SGC-7901 cell, suppression the activation of Akt or NF-kappaB can increase the effects of chemotherapeutics. NF-kappaB is a downstream target of Akt.

Melatonin reduces inflammatory injury through inhibiting NF-kappaB activation in rats with colitis.

Proinflammatory mediators are important in the pathogenesis of IBD, which are regulated by activation of NF-kappaB. The aim of this study was to investigate whether melatonin reduces inflammatory injury and inhibits proinflammatory molecule and NF-kappaB in rats with colitis. Rat colitis model was established by TNBS enema. NF-kappaB p65, TNF-alpha, ICAM-1, and IkappaBalpha in colon tissue were examined by immunohistochemistry, EMSA, RT-PCR, and Western blot analysis. Expression of proinflammatory molecule and activation of NF-kappaB were upregulated and IkappaB level decreased in rats with colitis. Melatonin reduces colonic inflammatory injury through downregulating proinflammatory molecule mediated by NF-kappaB inhibition and blockade of IkappaBalpha degradation.

Increased expression of RelA/nuclear factor-kappa B protein correlates with colorectal tumorigenesis.

OBJECTIVE: To identify the role of RelA/nuclear factor-kappa B, an important inhibitor of apoptosis in colorectal tumorigenesis, we examined the expression of RelA in normal colorectal mucosa (n = 10), colorectal adenomas (n = 30) and colorectal adenocarcinomas (n = 30). Furthermore, the association of RelA expression with tumor cell apoptosis, proliferation, and expression of Bcl-2/Bcl-x(L )was also studied. METHODS: Paraffin sections were stained with monoclonal antibodies directed against RelA, Bcl-2, Bcl-x(L), and Ki-67 to assess protein expression patterns in normal, adenomatous and colon cancer tissue. Apoptotic cells were detected by terminal deoxynucleotidyl-transferase-mediated dUTP-biotin nick end labeling (TUNEL) using an in situ detection kit. RESULTS: The results of immunohistochemical staining revealed that expression of RelA, Bcl-2, Bcl-x(L), and Ki-67 labeling index (LI) significantly increased in the transition from adenoma with low dysplasia to adenocarcinoma. This transition was associated with a significant decrease in the apoptotic index (AI) and a significant increase in the Ki-67 LI. The expression of RelA correlated inversely with the AI and correlated positively with the expression of Bcl-2, Bcl-x(L), and Ki-67 LI in the transition from low-grade dysplasia to adenocarcinoma. CONCLUSION: Our results suggest that increased expression of RelA/nuclear factor-kappa B plays an important role in the transition from colorectal adenoma with low-grade dysplasia to adenocarcinoma in the pathogenesis of colon cancer in humans.