Interstitial cystitis - intravesical treatment

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Pentosan polysulfide sodium for chronic non-bacterial prostatitis in the rat model / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the therapeutic effect of pentosan polysulfide sodium (PPS) on chronic non-bacterial prostatitis (CNP) in rats.</p><p><b>METHODS</b>Based on Robinette's method, we established a CNP model in 80 male SD rats, aged 6 months and weighing 315 - 450 g, by castration followed by subcutaneous injection of estradiol at 0.25 mg / (kg x d) for 30 consecutive days. Then we randomly allocated the model rats into a placebo group (n = 40) and a PPS group (n = 40) to receive intragastric administration of normal saline and PPS, respectively. After 8 weeks of treatment, the pathological changes in the rat prostatic tissue were observed by HE staining.</p><p><b>RESULTS</b>Varied degrees of chronic inflammation and inflammatory cell infiltration were seen in the prostatic tissues of both groups of rats before the treatment. The inflammation was significantly improved after the treatment in the PPS group but not in the placebo group.</p><p><b>CONCLUSION</b>PPS has some therapeutic effect on CNP in the rat, and its mechanism may be associated with the abilities of PPS to repair the damaged glycosaminoglycan layer and inhibit inflammation in the prostate.</p>

Potentiation of carbon tetrachloride hepatotoxicity by pentosan polysulfate in rats

Few data are available in the literature regarding the effect of pentosan polysulfate (PPS) on normal and fibrotic rat livers. In addition, the combination of PPS and carbon tetrachloride (CCl4) has not been studied so far. The objective of this study was to assess the effect of PPS on rat livers treated or not with CCl4 for the induction of liver fibrosis. The study consisted of four stages: 1) hepatic fibrosis induction with CCl4 (N = 36 rats); 2) evaluation of the effect of PPS on CCl4-induced hepatic fibrosis (N = 36 rats); 3) evaluation of the effect of higher doses of PPS in combination with CCl4 (N = 50 rats); 4) evaluation of the presence of an enzymatic inductor effect by PPS (N = 18 rats) using the sodium pentobarbital test which indirectly evaluates hepatic microsomal enzyme activity in vivo. Adult (60 to 70 days) male Wistar rats weighing 180 to 220 g were used. All animals receiving 0.5 ml 8 percent CCl4 (N = 36) developed hepatic fibrosis, and after 8 weeks they also developed cirrhosis. No delay or prevention of hepatic fibrosis was observed with the administration of 5 mg/kg PPS (N = 8) and 1 mg/kg PPS (N = 8) 1 h after the administration of CCl4, but the increased hepatotoxicity resulting from the combination of the two substances caused massive hepatic necrosis in most rats (N = 45). PPS (40 mg/kg) alone caused hepatic congestion only after 8 weeks, but massive hepatic necrosis was again observed in association with 0.5 ml CCl4 after 1 to 4 weeks of treatment. Unexpectedly, sleeping time increased with time of PPS administration (1, 2, or 3 weeks). This suggests that PPS does not function as an activator of the hepatic microsomal enzymatic system. Further studies are necessary in order to clarify the unexpected increase in hepatotoxicity caused by the combination of CCl4 and high doses of PPS, which results in massive hepatic necrosis

The impact of heterogeneity on the diagnosis and treatment of interstitial cystitis / O impacto da heterogeneidade no diagnóstico e tratamento da cistite intersticial

A cistite intersticial (CI) é uma doença cuja etiologia permanece desconhecida. A CI é um dos estados mais incômodos na prática urológica. Geralmente afeta mulheres, que apresenta sintomas de dor ao encherem a bexiga e freqüência urinária. A CI é uma síndrome heterogênea e é, freqüentemente, dividida em dois subtipos. Comparada à CI clássica, a do tipo näo-ulcerativa difere por apresentar aspectos sintomáticos, endoscópicos e histológicos diferentes, além da resposta aos vários tipos de tratamento. Esta revisäo é uma introduçäo à síndrome da CI, no que diz respeito a características clínicas e critérios de diagnóstico. Uma variedade de modalidades de tratamento têm sido sugeridas ao longo dos anos, e säo aqui revisadas e avaliadas, entre as quais estäo a hidrodistençäo da bexiga, a terapia de instilaçäo intravesical, a medicaçäo oral e a estimulaçäo elétrica transcutânea do nervo, a ressecçäo transuretral do tecido doente da bexiga, a cistectomia supratrigonal seguida de enterocistoplastia e derivaçäo urinário.

Evaluation of Biologic Phenotype by Midkine Gene Expression in Gastric Cancer as a Target for Biotherapy / 대한암학회지

PURPOSE: We studied biological phenotypes of gastric cancer cell lines based on a novel heparin-binding growth/differentiation factor, midkine (MK) expression. MATERIALS AND METHODS: Nine gastric cancer cell lines and 25 gastric cancer tissues were tested for MK expression by Northern blot analysis. Soft agar assay for in vitro tumorigenesis, cross- feeding assay for paracrine angiogenic activity, ELISA for uPA and PAI-1 measurement were performed. RESULTS: MK expression was found in 67% (6/9) of the gastric cancer cell lines, and 56% (14/25) of the primary gastric cancer tissues. Gastric cancer cell lines with MK expression were more tumorigenic in soft agar assay and endothelial cell growth stimulatory in cross-feeding assay than cells which did not express MK. However, urokinase-type plasminogen activator (uPA) expression did not correlate with MK expression. Growth of MK expressing cells was inhibited by a heparin-binding blocking agent, pentosan polysulfate (PPS). In cancer tissues, MK expression correlated with tumor size, suggesting in vivo autocrine and paracrine activity. CONCLUSION: Gastric cancer cells with increased MK gene expression showed increased tumorigenic and angiogenic activity. Therefore, this proliferation promoting activity of MK can be targeted by an anti-heparin binding agent as a biotherapy model in gastric cancer treatment.

Anti-tumor Effects of Growth Factor Inhibitors and Anti-metastatic Agents in Human Gastric Cancer Cell Lines / 대한암학회지

PURPOSE: For tumor growth, invasion and metastasis, a cascade of linked sequential biological events is essential; overproduction of growth factors, activation of proteolytic enzymes, induction of tumor angiogenesis, and enhanced tumor cell motility and attachment. We tried to test whether the biological therapy against the biological targets can modulate the specific biological characteristics, and furthermore increased anti-tumor effects can be induced when the biological therapy and cytotoxic chemotherapy were combined. MATERIALS AND METHODS: YCC-1, 2, 3, 7, and AGS human gastric cancer cell lines were used in these studies. Pentosan polysulfate (PPS) as a heparin-binding growth factor (HBGF) inhibitor, Tranexamic acid as a plasmin inhibitor, Adriamycin as a chemotherapeutic agent, were selected. The methods were Northern blot analysis for the detection of Midkine (MK) expression, soft agar assay for autocrine tumorigenicity. The expression of uPA, PAI-1 was determined by ELISA, while the MMPs activities were evaluated by zymography. The effects of each drug on tumorigenicity and tumor cell proliferation were evaluated by soft agar assay and cell proliferation assay, respectively. RESULTS: YCC-3, 7, AGS cell lines expressed MK mRNA, whereas YCC-1, 2 did not. YCC-2 cell line showed increased expression of uPA and MMP activities. Only MK expressing YCC-3 and 7 cell lines showed the tumorigenicity. PPS suppressed the colony forming activities as much as Adriamycin did (PPS; 8~24%, Adriamycin; 12~40%), but it showed only cytostatic effects in cell proliferation assay (PPS; 60~103%, Adriamycin; 22~97%). When PPS was combined with Adriamycin on the Adriamycin resistant, MK expressing YCC-7 cell line, the growth inhibition rate increased up to 84%, while that of PPS or Adriamycin single treatment was 40%, 22%, respectively (p=0.001). CONCLUSION: The modulation of specific biological targets can induce the anti-tumor effects. This suggests the possible clinical application of biological therapy in gastric cancer.