Capsaicin Inhibits Inflammation and Gastric Damage during H pylori Infection by Targeting NF-kB–miRNA Axis

Saha, Kalyani; Sarkar, Deotima; Khan, Uzma; Karmakar, Bipul Chandra; Paul, Sangita; Mukhopadhyay, Asish K.; Bhattacharya, Sushmita

doi:10.3390/pathogens11060641

Cited by 15 publications

(12 citation statements)

References 53 publications

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“…The transcription factor NF-κB is one of the major mediators of the inflammatory response against H. pylori infection [ 75 ]. H. pylori activates NF-κB through the canonical pathway, namely IKK complex phosphorylation/degradation of the IκB inhibitor, leading to the nuclear translocation of NF-κB, and thereby resulting in the acceleration of its target genes [ 15 , 68 , 76 ]. In this study, we showed that KP reduced the phosphorylation of IκBα and p65, thereby repressing the translocation of p65 from the cytosol to the nucleus in H. pylori -infected gastric mucosal injury mice.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effect of Korean Propolis on Helicobacter pylori-Infected Gastric Mucosal Injury Mice Model

et al. 2022

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Propolis, a natural resinous substance obtained from a variety of buds and plants, has been reported to possess various biological functions. Several recent studies have demonstrated the inhibitory effects of propolis on the growth of Helicobacter pylori (H. pylori) in vitro; however, current research efforts on Korean propolis (KP) remain insufficient especially in vivo. Our study aims to investigate the anti-inflammatory effect and molecular mechanism of KP on mouse gastric mucosa during H. pylori infection. We examined an in vivo H. pylori-induced gastric mucosal injury mice model. We found that KP inhibited the growth of H. pylori and attenuated the expression of H. pylori virulence factors such as cytotoxin-associated gene A, encoding urease A subunit, surface antigen gene and neutrophil-activating protein A. Moreover, KP reduced both gross lesions and pathological scores in H. pylori-challenged mice. In addition, KP markedly restrained the production of pro-inflammatory cytokines and nitric oxide levels compared with an untreated H. pylori-infected group. In particular, we found that KP repressed the phosphorylation of IκBα and NF-κB p65 subunit, and subsequently suppressed their downstream target genes. Taken together, these findings demonstrate the beneficial effects of KP on inflammation through the inhibition of NF-κB signaling as well as inhibition of H. pylori growth in a mouse model infected with H. pylori. This suggests the potential application of KP as a natural supplement for patient’s suffering from gastric mucosal injury caused by H. pylori infection.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effect of Korean Propolis on Helicobacter pylori-Infected Gastric Mucosal Injury Mice Model

et al. 2022

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“…Helicobacter pylori , Sydney Strain SS1 ( cagA + , vacA s2m2) were grown on brain heart infusion (BHI) agar (Difco, USA) containing 7% heat-inactivated horse serum (Invitrogen), antibiotics, and IsoVitaleX as mentioned previously (Saha et al 2022 ). Plates were kept in a microaerophilic atmosphere at 37 °C for five to six days.…”

Section: Methodsmentioning

confidence: 99%

“…At the end of week 4, all mice were sacrificed. Gastric tissues were isolated and blood was collected for experimental purposes as described previously (Saha et al 2022 ). Experiments were repeated three times.…”

Section: Methodsmentioning

confidence: 99%

Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infection

Khan

Karmakar

Basak

et al. 2023

Mol Med

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Background Helicobacter pylori is a key agent for causing gastric complications linked with gastric disorders. In response to infection, host cells stimulate autophagy to maintain cellular homeostasis. However, H. pylori have evolved the ability to usurp the host’s autophagic machinery. High mobility group box1 (HMGB1), an alarmin molecule is a regulator of autophagy and its expression is augmented during infection and gastric cancer. Therefore, this study aims to explore the role of glycyrrhizin (a known inhibitor of HMGB1) in autophagy during H. pylori infection. Main methods Human gastric cancer (AGS) cells were infected with the H. pylori SS1 strain and further treatment was done with glycyrrhizin. Western blot was used to examine the expression of autophagy proteins. Autophagy and lysosomal activity were monitored by fluorescence assays. A knockdown of HMGB1 was performed to verify the effect of glycyrrhizin. H. pylori infection in in vivo mice model was established and the effect of glycyrrhizin treatment was studied. Results The autophagy-lysosomal pathway was impaired due to an increase in lysosomal membrane permeabilization during H. pylori infection in AGS cells. Subsequently, glycyrrhizin treatment restored the lysosomal membrane integrity. The recovered lysosomal function enhanced autolysosome formation and concomitantly attenuated the intracellular H. pylori growth by eliminating the pathogenic niche. Additionally, glycyrrhizin treatment inhibited inflammation and improved gastric tissue damage in mice. Conclusion This study showed that inhibiting HMGB1 restored lysosomal activity to ameliorate H. pylori infection. It also demonstrated the potential of glycyrrhizin as an antibacterial agent to address the problem of antimicrobial resistance.

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“…H. pylori , Sydney Strain SS1 (cagA+, vacA s2m2) were grown on brain heart infusion (BHI) agar (Difco, USA) containing 7% heat-inactivated horse serum (Invitrogen), antibiotics and IsoVitaleX as mentioned previously (33). Plates were kept in a microaerophilic atmosphere at 37°C for five to six days.…”

Section: H Pylori Culturementioning

confidence: 99%

Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits H. pylori infection

Khan

Karmakar

Basak

et al. 2022

Preprint

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Helicobacter pylori a key agent for causing gastric complications is linked with peptic ulcer, gastritis, and in severe cases gastric cancer. In response to infection, host cells stimulate autophagy to maintain cellular homeostasis. However, H. pylori have evolved the ability to usurp the host's autophagic machinery. High mobility group box1 (HMGB1), an alarmin molecule is a regulator of autophagy and its expression is augmented in gastric cancer and many other cancers. Therefore, this study aims to explore the role of glycyrrhizin (a known inhibitor of HMGB1) in autophagy during H. pylori infection. Human gastric cancer (AGS) cells were infected with H. pylori SS1 strain and further treatment was done with glycyrrhizin. Western blot was used to examine the expression levels of autophagy proteins. Autophagy and lysosomal activity were monitored by immunofluorescence. We have performed knockdown of HMGB1 to verify the effect of glycyrrhizin by siRNA transfection method. H. pylori-infection in vivo C56BL/6 mice model was established and the effect of glycyrrhizin treatment was studied. We found that the autophagy-lysosomal pathway was impaired due to a significant increase in lysosomal membrane permeabilization during H. pylori infection in AGS cells. Subsequently, glycyrrhizin treatment restored the lysosomal membrane integrity, accompanied by an increase in cathepsin B activity and reduction of ROS and inflammatory cytokine IL-8. The recovered lysosomal function enhanced autolysosome formation and concomitantly attenuated the intracellular H. pylori growth by eliminating the pathogenic niche from gastric cells. Additionally, glycyrrhizin treatment inhibited inflammation and improved gastric tissue damages in mice.

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Capsaicin Inhibits Inflammation and Gastric Damage during H pylori Infection by Targeting NF-kB–miRNA Axis

Cited by 15 publications

References 53 publications

Anti-Inflammatory Effect of Korean Propolis on Helicobacter pylori-Infected Gastric Mucosal Injury Mice Model

Anti-Inflammatory Effect of Korean Propolis on Helicobacter pylori-Infected Gastric Mucosal Injury Mice Model

Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infection

Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits H. pylori infection

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