Assessing the toxic effects of hydroalcoholic extract of Stachys lavandulifolia Vahl on rat's liver

Aims: Stachys lavandulifolia Vahl is a frequently used plant to treat different diseases, but its probable toxic effects have not been reported yet. This study aimed to study the toxicity of the extract on rats' liver. Methods: In this experimental study, 100 rats were designated into 10 groups and injected normal saline or Stachys lavandulifolia Vahl extract at 50, 100, 150, and 200 mg/kg, intraperitoneally for 28 days. Four case groups and one control group were examined for ALT, AST and ALP after one month and the other groups were evaluated after two months. Results: In the first month, the increase of ALP at all doses and the increase of AST at 200 mg/kg was significant, compared to the control group (p<0.05). In the second month, AST increased at the dosage of 150mg/kg, and ALP decreased at the dosage of 100 mg/kg, compared to the control group (p<0.05). Histopathological assessment showed a significant dose dependent increase both in necrotic-inflammatory reactions and fibrotic lesions, in the first and second months, compared to the control group (p<0.001). Conclusions: The Stachys lavandulifolia extract injected intraperitoneally has hepatotoxic effect, which is not eliminated by the drug withdrawal. Therefore, it is necessary to be consumed with caution (Tab. 4, Fig. 1, Ref 21). Text in PDF www.elis.sk

Association of the virulence factors of Helicobacter pylori and gastric mucosal interleukin-17/23 mRNA expression in dyspeptic patients

The molecular pathways that control Helicobacter pylori (Hp)-associated inflammatory reaction are complex, but locally induced cytokines and virulence factors seem to have a major role in maintaining the ongoing inflammation. Therefore this study was aimed to evaluate the association of the virulence factors of Hp and gastric mucosal interleukin-17/23 mRNA expression in dyspeptic patients. Mucosal IL-17 and IL-23 mRNA expression in H. pylori infected and non-infected gastric biopsies were determined by real-time RT-PCR. Virulence factors, vac-A and cag-A were evaluated using PCR. There was no significant difference in mucosal IL-17 and IL-23 mRNA expression between H. pylori infected and non-infected patients. Their expression in mucosa did not correlate with chronic gastritis and chronic active gastritis. IL-17 and IL-23 mRNA expression in mucosa of patients with vacA m1 were significantly higher than those observed in patients with vacA m2. The severity of polymorphonuclear infiltration and chronic active gastritis was higher in cag-A positive than cag-A negative patients. H. pylori infections carrying the vacA m1 allele have higher IL-17 and IL-23 mRNA and the current study suggests that the virulence factor vacA allele’s m1 are important for the severe gastric inflammation

Mucosal interleukin-21 mRNA expression level is high in patients with Helicobacter pylori and is associated with the severity of gastritis

Helicobacter pylori (H. pylori) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells. Different clinical forms of the infection may reflect distinctive patterns of cytokine expression. Interleukin (IL)-17, IL-21, IL-22, and IL-23 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relationship to different patterns of inflammation and virulence factors remain unclear. The present study was launched to analyse IL-6 expression in H. pylori-infected and uninfected gastric patients and to investigate its correlation with chronic gastritis among H. pylori-infected patients. Total RNA was extracted from the gastric antrum biopsies of 48 H. pylori-infected patients and 38 H. pylori uninfected patients. Mucosal IL-21 mRNA expression level in H. pylori-infected and uninfected gastric biopsy was determined by real-time PCR. The presence of vacA (vacuolating cytotoxin A) and cagA (cytotoxin associated gene A) virulence factors were evaluated using PCR. Interleukin-21 mRNA expression was significantly high in biopsies of H. pylori-infected patients compared to H. pylori uninfected patients, and the mucosal IL-21 mRNA level was positively correlated with the grade of chronic inflammation. There was no association between virulence factors and IL-21 mRNA expression. We believe that IL-21 might be involved in the pathogenesis of H. pylori and might be an index of the severity of chronic gastritis

Expression of IL-18 cytokine mRNA in gastric mucosa tissue of patients with H. pylori infection in Chahar Mahal and Bakhtiari

Background: H. pylori infection is associated with gastritis and marked infiltration of the gastric mucosa by inflammatory cells secreting of several cytokines that contribute to maintain and expand the local inflammation. Different clinical expressions of the infection may reflect different patterns of cytokine expression. Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-17, IL-23, and IL-18 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relation to different patterns of inflammation remain unclear. Materials and Methods: Analysis of IL-18 RNA transcripts was performed by real-time PCR. Total RNA was extracted from gastric biopsies of 56 H. pylori-infected patients, 50 H. pylori-negative patients with gastritis, by biozol reagent according to the manufacturer's instructions. CDNA was synthesized from 1 mg of total RNA using First Strand cDNA Synthesis Kit (fermentas) and 3 μL cDNA was amplified by PCR using the 2x Rotor-Gene Probe PCR Master Mix (QIAGEN) and specific primers for each cytokine and β-actin. Results: IL-18 mRNA expression was significantly increased in biopsies of H. pylori-infected patients compared to H. pylori-uninfected individuals. Conclusion: IL-18 may play an important role in the inflammatory response and promoting gastric Th1 responses to H. pylori colonization, and may ultimately influence the outcome of H. pylori-associated diseases that arise within the context of gastritis

The Hepatotoxic Effects of Stachys Lavandulifolia Vahl on Wistar Rat

Background and purpose: Stachys lavandulifolia is a plant commonly used for many diseases. But so far there is no report indicating its toxicity. The aim of this study was to investigate the probable hepatoxicity of S. lavandulifolia extract on Wistar rats. Materials and methods: In this experimental study, 100 Wistar rats (about 250gr, 8-12 weeks old) were randomly divided into 10 groups (8 groups as case and 2 groups as control). They were intraperitoneally injected with S. lavandulifolia extract with doses of 50, 100, 150 and 200mg/kg per day for 28 days. Afterwards, the serum parameters level (ALP, AST, ALT) and pathological samples were evaluated and compared in four case group and one control group after 28 days and other groups after one month. Results: On the first month there was significant increase on AST level only in 200mg/kg dose while ALP level significantly increased in all doses (P<0.05). There was no significant difference among all doses regarding their effects on the increase of liver enzymes (P>0.05). On the second month, the changes in liver enzymes were almost the same as first month, except 150mg/kg dose that significantly increased the AST level compared to control group and also this dose significantly increased the ALP level compared to 100mg/kg dose (P<0.05). In examining liver samples obtained from rats in the first and second months, necrotic inflammatory reactions and fibrotic lesions significantly increased compared to control group (P<0.001). In the first month we also found that there was significant difference between higher doses (150 and 200mg/kg) and lower doses (50 and 100mg/kg) regarding their effects on hepatic lesion (P<0.05). Conclusion: Since the extract of S. lavandulifolia causes toxicity it should be consumed with caution in people with underlying cholestatic diseases

Virulence factors of Helicobacter pylori vacA increase markedly gastric mucosal TGF-beta 1 mRNA expression in gastritis patients

Objective: Helicobacter pylori (H. pylori) infection is the main cause of gastric inflammation. Regulatory T cells (Treg cells) suppress the activation and proliferation of antigen-specific T cells and mediate immunologic tolerance. TGF-beta 1 was shown to be secreted in a subset of Treg cells known as `Th3 cells'. These cells have not been sufficiently studied in context to H. pylon-induced inflammation in human gastric mucosa. In this study we therefore, aimed to investigate the expression of TGF-beta 1 in the context of H. pylori colonization in chronic gastritis, to examine the relationship between it and histopathologic findings and to compare it with virulence factors. Patients and methods: Total RNA was extracted from gastric biopsies of 48 H. pylori-infected patients and 38 H. pylori-negative patients with gastritis. Mucosal TGF-beta 1 mRNA expression in H. pylori-infected and uninfected gastric biopsies was determined by real-time PCR. Presence of vacA, cagA, iceA, babA2 and oipA virulence factors was evaluated using PCR. Results: TGF-beta 1 mRNA expression was significantly increased in biopsies of H. pylori-infected patients compared to H. pylori-uninfected patients. There was association between virulence factors and TGF-beta 1 mRNA expression. TGF-beta 1 mRNA expression in mucosa was significantly higher in patients with vacA s1 and s1m1. Conclusions: TGF-beta 1 may play an important role in the inflammatory response and promote the chronic and persistent inflammatory changes in the gastric. This may ultimately influence the outcome of H. pylon-associated diseases that arise within the context of gastritis and vacA may suffice to induce expression of TGF-beta 1 mRNA. (C) 2014 Elsevier Ltd. All rights reserved

Expression levels of mRNA cytokines of IL-17 and IL-23 in epithelialfiber of stomach inpatients with Helicobacter pylori using Real-Time PCR in Chahar Mahal and Bakhtiari province

زمینه و هدف: اینترلوکین های 17 و 23 در دفاع بر علیه برخی عفونت‌های مخاطی دستگاه گوارش نقش دارند و IL-17 باعث جذب نوتروفیل ها به محل عفونت شده و در ایجاد التهاب نقش دارد. مطالعه حاضر میزان بیان mRNA سیتوکاین های IL-17و IL-23در دو گروه بیماران گاستریتی با عفونت هلیکوباکترپیلوری و فاقد عفونت را به وسیله روش کمی Real-Time PCR بررسی می‌کند. روش بررسی: در این مطالعه مورد- شاهدی، از 58 بیمار دارای گاستریت با عفونت هلیکوباکترپیلوری و 50 بیمار مبتلا به گاستریت که فاقد عفونت بودند، توسط آندوسکوپی بیوپسی تهیه شد. بعد از استخراجmRNA و تبدیل آن به cDNA، میزان بیانmRNA مربوط به IL-17و IL-23در نمونه‌ها توسط Real-Time PCR اندازه گیری شد و بیان سایتوکاین ها در دو گروه آلوده و غیر آلوده با استفاده از تست Mann–Whitney مورد آنالیز قرار گرفت. یافته‌ها: ارتباط معنی‌داری بین میزان بیانIL-17 mRNA در افراد دارای گاستریت با عفونت هلیکوباکترپیلوری و افراد دارای گاستریت فاقد عفونت دیده نشد (941/0P=). همچنین ارتباط بین میزان بیان mRNA IL-23در بیماران دارای گاستریت با عفونت هلیکوباکترپیلوری و بیماران دارای گاستریت فاقد عفونت معنی دار نبود (076/0 P=). نتیجه‌گیری: نتایج این مطالعه نشان داد که میزان بیان mRNA سیتوکاین های IL-17و IL-23در بیماران دارای گاستریت با عفونت هلیکوباکترپیلوری در مقایسه با بیماران گاستریتی بدون عفونت بالاتر نمی‌باشد و در نتیجه ارتباط معنی داری بین دو گروه مورد مطالعه در این استان وجود ندارد؛ لذا می طلبد تا نقش دقیق سایتوکاین ‌های دیگر درگیر در بروز بیماری گاستریت جهت تعیین پیش آگهی و ارزیابی برنامه های درمانی بیشتر مشخص شود

Association between virulence factors of helicobacter pylori and gastric mucosal interleukin-18 mRNA expression in dyspeptic patients

Background: Helicobacter pylori (Hp) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells that contribute to sustain and expand the local inflammation. Different clinical expressions of the infection may reflect distinctive patterns of cytokine expression. IL-1 beta, TNF-alpha, IL-17 and IL-23 have been reported to be involved in Hp-induced gastric mucosal inflammation, but the details and association to different patterns of inflammation and virulence factors remain unclear. Methods: Total RNA was extracted from gastric biopsies of 51 Hp-infected patients and 44 Hp-negative patients. Mucosal IL-18 mRNA expression in gastric biopsies was determined by Real-Time PCR. Presence of virulence factors was evaluated using PCR. Results: IL-18 mRNA expression was significantly increased in biopsies of Hp-infected patients compared to Hp-uninfected individuals. There was no association between virulence factors and IL-18 mRNA expression. Also severity of mononuclear infiltration was significantly higher in gastritis patients with vacA (m1)-positive compare patients with vacA (m2)-positive. Conclusions: IL-18 may play an important role in the inflammatory response and promote the chronic and persistent inflammatory changes in the stomach. This may ultimately influence the outcome of Hp-associated diseases that arise within the context of gastritis. (C) 2013 Elsevier Ltd. All rights reserved

Assessing the toxic effects of hydroalcoholic extract of Stachys lavandulifolia Vahl on rat’s liver

Aims: Stachys lavandulifolia Vahl is a frequently used plant to treat different diseases, but its probable toxic effects have not been reported yet. This study aimed to study the toxicity of the extract on rats' liver. Methods: In this experimental study, 100 rats were designated into 10 groups and injected normal saline or Stachys lavandulifolia Vahl extract at 50, 100, 150, and 200 mg/kg, intraperitoneally for 28 days. Four case groups and one control group were examined for ALT, AST and ALP after one month and the other groups were evaluated after two months. Results: In the first month, the increase of ALP at all doses and the increase of AST at 200 mg/kg was significant, compared to the control group (p<0.05). In the second month, AST increased at the dosage of 150mg/kg, and ALP decreased at the dosage of 100 mg/kg, compared to the control group (p<0.05). Histopathological assessment showed a significant dose dependent increase both in necrotic-inflammatory reactions and fibrotic lesions, in the first and second months, compared to the control group (p<0.001). Conclusions: The Stachys lavandulifolia extract injected intraperitoneally has hepatotoxic effect, which is not eliminated by the drug withdrawal. Therefore, it is necessary to be consumed with caution (Tab. 4, Fig. 1, Ref 21). Text in PDF www.elis.sk

Virulence factors of Helicobacter pylori vacA increase markedly gastric mucosal TGF-β1 mRNA expression in gastritis patients

Objective: Helicobacter pylori (H. pylori) infection is the main cause of gastric inflammation. Regulatory T cells (Treg cells) suppress the activation and proliferation of antigen-specific T cells and mediate immunologic tolerance. TGF-b1 was shown to be secreted in a subset of Treg cells known as ‘Th3 cells’. These cells have not been sufficiently studied in context to H. pylori-induced inflammation in human gastric mucosa. In this study we therefore, aimed to investigate the expression of TGF-b1 in the context of H. pylori colonization in chronic gastritis, to examine the relationship between it and histopathologic findings and to compare it with virulence factors. Patients and methods: Total RNA was extracted from gastric biopsies of 48 H. pylori-infected patients and 38 H. pylori-negative patients with gastritis. Mucosal TGF-b1 mRNA expression in H. pylori-infected and uninfected gastric biopsies was determined by real-time PCR. Presence of vacA, cagA, iceA, babA2 and oipA virulence factors was evaluated using PCR. Results: TGF-b1 mRNA expression was significantly increased in biopsies of H. pylori-infected patients compared to H. pylori-uninfected patients. There was association between virulence factors and TGF-b1 mRNA expression. TGF-b1 mRNA expression in mucosa was significantly higher in patients with vacA s1 and s1m1. Conclusions: TGF-b1 may play an important role in the inflammatory response and promote the chronic and persistent inflammatory changes in the gastric. This may ultimately influence the outcome of H. pylori-associated diseases that arise within the context of gastritis and vacA may suffice to induce expression of TGF-b1 mRNA