Background and ObjectiveThis study was aimed to elucidate the molecular mechanism of Momordica charantia (MCh), along with a standard drug prednisolone, in a rat model of colitis induced by trinitrobenzene sulfonic acid (TNBS).MethodsAfter the induction of the experimental colitis, the animals were treated with MCh (4 g/kg/day) for 14 consecutive days by intragastric gavage. The colonic tissue expression levels of C-C motif chemokine ligand 17 (CCL-17), interleukin (IL)-1β, IL-6, IL-23, interferon-γ (IFN-γ), nuclear factor kappa B (NF-kB), and tumor necrosis factor-α (TNF-α), were determined at both mRNA and protein levels to estimate the effect of MCh. Besides, colonic specimens were analyzed histopathologically after staining with hematoxylin and eosin.ResultsThe body weights from TNBS-instigated colitis rats were found to be significantly lower than untreated animals. Also, the IFN-γ, IL-1β, IL-6, Il-23, TNF-α, CCL-17, and NF-kB mRNA and protein levels were increased significantly from 1.86-4.91-fold and 1.46-5.50-fold, respectively, in the TNBS-instigated colitis group as compared to the control. Both the MCh and prednisolone treatment significantly reduced the bodyweight loss. It also restored the induced colonic tissue levels of IL-1β, IL-6, IFN-γ, and TNF-α to normal levels seen in untreated animals. These results were also supported with the histochemical staining of the colonic tissues from both control and treated animals.ConclusionThe presented data strongly suggests that MCh has the anti-inflammatory effect that might be modulated through vitamin D metabolism. It is the right candidate for the treatment of UC as an alternative and complementary therapeutics.

Objectives Cellular interactions and cell adhesion underlie preeclampsia (PE). The aim of the current study is to investigate the role of cell adhesion molecules such as CD97, neural (N)-cadherin, epithelial (E) -cadherin and integrin beta-4 in PE. Methods This prospective study included 20 pregnant women with PE and a control group of 16 healthy pregnant women who were matched for age, gestational age, gravida and parity. Standard blood tests and placental cell adhesion molecule immunohistochemical staining were examined. Results The creatinine, uric acid and lactate dehydrogenase (LDH) levels from standard blood tests were found to be statistically higher in the PE group (p = 0.002, p = 0.000, p = 0.001; respectively). In the PE group, the CD97 maternal serum level was statistically significantly lower, as was its immunohistochemical expression in placental sections (p = 0.028, p = 0.000; respectively). The E-cadherin expression score was statistically higher in the PE group compared to the control group (3,65 ± 1,84 vs 2,06 ± 1,76 respectively; p = 0.003). The N-cadherin expression score was statistically lower in the PE group compared to the control group (1,50 ± 0,82 vs 2,43 ± 1,59 respectively; p = 0.049). Integrin beta-4 was not statistically different between groups. Conclusions Cellular interaction may be responsible for PE as in cancer. A balance in intercellular communication, as researched in cancer therapy, may offer the solution in PE.

Objectives: Cellular interactions and cell adhesion underlie preeclampsia (PE). The aim of the current study is to investigate the role of cell adhesion molecules such as CD97, neural (N)-cadherin, epithelial (E) -cadherin and integrin beta-4 in PE. Methods: This prospective study included 20 pregnant women with PE and a control group of 16 healthy pregnant women who were matched for age, gestational age, gravida and parity. Standard blood tests and placental cell adhesion molecule immunohistochemical staining were examined. Results: The creatinine, uric acid and lactate dehydrogenase (LDH) levels from standard blood tests were found to be statistically higher in the PE group (p=0.002, p=0.000, p=0.001; respectively). In the PE group, the CD97 maternal serum level was statistically significantly lower, as was its immunohistochemical expression in placental sections (p=0.028, p=0.000; respectively). The E-cadherin expression score was statistically higher in the PE group compared to the control group (3,65±1,84 vs 2,06±1,76 respectively; p=0.003). The N-cadherin expression score was statistically lower in the PE group compared to the control group (1,50±0,82 vs 2,43±1,59 respectively; p=0.049). Integrin beta-4 was not statistically different between groups. Conclusions: Cellular interaction is responsible for PE as in cancer. A balance in intercellular communication, as researched in cancer therapy, may offer the solution in PE. Keywords: Preeclampsia, Cadherins, CD97, E-cadherin, N-cadherin, Integrin beta-4

Objectives Cellular interactions and cell adhesion underlie preeclampsia (PE). The aim of the current study is to investigate the role of cell adhesion molecules such as CD97, neural (N)-cadherin, epithelial (E) -cadherin and integrin beta-4 in PE. Methods This prospective study included 20 pregnant women with PE and a control group of 16 healthy pregnant women who were matched for age, gestational age, gravida and parity. Standard blood tests and placental cell adhesion molecule immunohistochemical staining were examined. Results The creatinine, uric acid and lactate dehydrogenase (LDH) levels from standard blood tests were found to be statistically higher in the PE group (p = 0.002, p = 0.000, p = 0.001; respectively). In the PE group, the CD97 maternal serum level was statistically significantly lower, as was its immunohistochemical expression in placental sections (p = 0.028, p = 0.000; respectively). The E-cadherin expression score was statistically higher in the PE group compared to the control group (3,65 ± 1,84 vs 2,06 ± 1,76 respectively; p = 0.003). The N-cadherin expression score was statistically lower in the PE group compared to the control group (1,50 ± 0,82 vs 2,43 ± 1,59 respectively; p = 0.049). Integrin beta-4 was not statistically different between groups. Conclusions Cellular interaction is responsible for PE as in cancer. A balance in intercellular communication, as researched in cancer therapy, may offer the solution in PE.

Gün geçtikçe artmakta olan kanser çağımızın ciddi global sağlık sorunudur ve akciğer kanseri tüm dünyada toplam kanser sayısı içerisinde en sık görülen kanserdir. Tümörlerin gelişiminde ve metastazında anjiogenez önemli bir rol oynamaktadır. Farklı endotel belirteçleri ile hesaplanan mikrodamar yoğunluğunun (MY) bazı tümörlerde kötü prognoz ve ileri evre ile ilişkili olduğu gösterilmiştir ve buradan hareketle metastazı öngörebileceği ileri sürülmüştür. Çalışmamızda, küçük hücreli dışı akciğer kanserlerinde (KHDAK) MY'yi immünohistokimyasal olarak endoglin, CD31 ve VEGFR2 ile tespit edip, serum endoglin seviyesi ile ilişkilendirerek sonuçlarımızı akciğer tümörlerinin progresyonu ile karşılaştırmayı amaçladık. Gereç ve yöntem: Çalışmamızda 36 skuamöz hücreli karsinom (SHK) ve 36 adenokarsinom olmak üzere toplam 72 akciğer dokusunda anjiogenik faktörlerden endoglin (CD105), CD31, VEGFR2'nin ekspresyonu immünohistokimyasal olarak incelendi. Primer akciğer kanseri tanısı alan gönüllü 26 kişinin ve 26 sağlıklı gönüllüden alınan serumlarda endoglin seviyesi Elisa yöntemi ile tespit edildi. Bulgular: Endoglinin aktive edilmiş endotelyal hücreleri için daha büyük bir afiniteye sahip olduğunu gözledik. Her iki tümör tipinde CD31 nonspesifik boyanma göstermiş MY daha zor tespit edilmiştir. VEGFR2 boyalı kesitlerde tümör içinde ve dışındaki damar duvarlarında yaygın pozitiflik saptandı. Serum endoglin seviyesinin KHDAK hastaları ile kontrol grubu arasında istatistiksel olarak anlamlı olmadığı tespit edildi. İmmünohistokimyasal olarak endoglin, CD31 ve VEGFR2 ekspresyonu ile sağkalım arasında istatistiksel olarak anlamlılık mevcut değildi. Sonuç: Çalışmamız sonucunda KHDAK'de immünohistokimyasal olarak spesifik boyanan endoglinin SHK ve adenokarsinom tipli hastalarda anjiogenezin değerlendirilmesinde daha iyi bir belirteç olabileceğini düşünmekteyiz.Anahtar kelimeler: Küçük hücreli dışı akciğer kanseri (KHDAK), anjiogenez, endoglin, CD31, VEGFR2.