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Protection of Gastrointestinal Mucosa from Acute Heavy Alcohol Consumption: The Effect of Berberine and Its Correlation with TLR2, 4/IL1β-TNFα Signaling.

Wang XP, Lei F, Du F, Chai YS, Jiang JF, Wang YG, Yu X, Yan XJ, Xing DM, Du LJ - PLoS ONE (2015)

Bottom Line: The purpose of the present study is to confirm the protective effect of berberine (BBR) on gastrointestinal injury caused by acute heavy alcohol exposure, an effect that has not been reported previously.Acute high alcohol concentrations lead to obvious damage to the gastrointestinal mucosa, resulting in necrosis of the intestinal mucosa.Oral administration of BBR was able to significantly reduce this alcohol-induced damage, inhibit increases of alcohol-induced TNFα and IL-1β expression in gastrointestinal mucosa as well as their upstream signals TLR2 and TLR4, and regulate cytokines that modulate tight junctions.

View Article: PubMed Central - PubMed

Affiliation: MOE Key Laboratory of Protein Sciences, Laboratory of Molecular Pharmacology and Pharmaceutical Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China.

ABSTRACT
The purpose of the present study is to confirm the protective effect of berberine (BBR) on gastrointestinal injury caused by acute heavy alcohol exposure, an effect that has not been reported previously. Our research details how BBR protects against gastrointestinal injuries from acute alcohol exposure using both in vivo and in vitro experiments. Acute high alcohol concentrations lead to obvious damage to the gastrointestinal mucosa, resulting in necrosis of the intestinal mucosa. Oral administration of BBR was able to significantly reduce this alcohol-induced damage, inhibit increases of alcohol-induced TNFα and IL-1β expression in gastrointestinal mucosa as well as their upstream signals TLR2 and TLR4, and regulate cytokines that modulate tight junctions. Alcohol consumption is a popular human social behavior worldwide, and the present study reports a comprehensive mechanism by which BBR protects against gastrointestinal injuries from alcohol stress, providing people with a novel application of BBR.

No MeSH data available.


Related in: MedlinePlus

General observation and morphology of gastro-intestines after acute alcohol exposure (H.E. staining).Berberine (BBR) was administered at three different doses of 75, 150 and 300 mg/kg. A 60% alcohol was employed. The alcohol was administered at dose of 0.15 ml/10g body weight. The arrows indicate congestive necrosis places. (A): Observation of stomach and small intestines. Intestinal congestion occurs in the duodenum in model mouse. (B): Morphology of small intestines after alcohol administration. In the mouse model, small intestinal mucosa appears necrosis. BBR could prevent alcohol injury from the intestines. (C): Morphology of stomach after alcohol exposure. (D): Mucosa of small intestines (magnified 200 times). Alcohol causes gastric mucosal injury, edema with light staining. (E): Statistical score of the histopathological diagnoses for small intestines injury after alcohol consumption. Kruskal-Wallis chi-squared = 24.0696, df = 4, P = 7.735e-05. Data are expressed as the mean ± S.D. from six different mice. ###, vs. normal mice, P < 0.001. **, vs. model mice, P < 0.01.
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pone.0134044.g001: General observation and morphology of gastro-intestines after acute alcohol exposure (H.E. staining).Berberine (BBR) was administered at three different doses of 75, 150 and 300 mg/kg. A 60% alcohol was employed. The alcohol was administered at dose of 0.15 ml/10g body weight. The arrows indicate congestive necrosis places. (A): Observation of stomach and small intestines. Intestinal congestion occurs in the duodenum in model mouse. (B): Morphology of small intestines after alcohol administration. In the mouse model, small intestinal mucosa appears necrosis. BBR could prevent alcohol injury from the intestines. (C): Morphology of stomach after alcohol exposure. (D): Mucosa of small intestines (magnified 200 times). Alcohol causes gastric mucosal injury, edema with light staining. (E): Statistical score of the histopathological diagnoses for small intestines injury after alcohol consumption. Kruskal-Wallis chi-squared = 24.0696, df = 4, P = 7.735e-05. Data are expressed as the mean ± S.D. from six different mice. ###, vs. normal mice, P < 0.001. **, vs. model mice, P < 0.01.

Mentions: Two hours after 60% alcohol administration, the alcohol-induced pathological damage was observed as a congestive and dark red appearance in the duodenum compared with that of normal mice. High-dose BBR (300mg/kg) effectively inhibited the alcohol-induced morphological changes of the duodenum (Fig 1A). By light microscopy, congestion, edema, necrosis and shedding of the mucosa from duodenum was observed in alcohol-treated mice (Fig 1B and 1D). BBR was able to effectively antagonize the alcohol-induced pathological changes in the duodenum, which was indistinguishable in morphology from the saline group. Unlike the small intestine, the gastric mucosa exhibited minor pathological changes among the different groups (Fig 1C). It has previously been reported that 100% alcohol can cause erosion in rat stomach mucosa and can up-regulate the mRNA expression of c-fos, c-jun and HSP70 in the damaged epithelium; however, the necrosis in the stomach was less severe than in the small intestine[27], suggesting that the small intestines were more sensitive to alcohol damage.


Protection of Gastrointestinal Mucosa from Acute Heavy Alcohol Consumption: The Effect of Berberine and Its Correlation with TLR2, 4/IL1β-TNFα Signaling.

Wang XP, Lei F, Du F, Chai YS, Jiang JF, Wang YG, Yu X, Yan XJ, Xing DM, Du LJ - PLoS ONE (2015)

General observation and morphology of gastro-intestines after acute alcohol exposure (H.E. staining).Berberine (BBR) was administered at three different doses of 75, 150 and 300 mg/kg. A 60% alcohol was employed. The alcohol was administered at dose of 0.15 ml/10g body weight. The arrows indicate congestive necrosis places. (A): Observation of stomach and small intestines. Intestinal congestion occurs in the duodenum in model mouse. (B): Morphology of small intestines after alcohol administration. In the mouse model, small intestinal mucosa appears necrosis. BBR could prevent alcohol injury from the intestines. (C): Morphology of stomach after alcohol exposure. (D): Mucosa of small intestines (magnified 200 times). Alcohol causes gastric mucosal injury, edema with light staining. (E): Statistical score of the histopathological diagnoses for small intestines injury after alcohol consumption. Kruskal-Wallis chi-squared = 24.0696, df = 4, P = 7.735e-05. Data are expressed as the mean ± S.D. from six different mice. ###, vs. normal mice, P < 0.001. **, vs. model mice, P < 0.01.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4520689&req=5

pone.0134044.g001: General observation and morphology of gastro-intestines after acute alcohol exposure (H.E. staining).Berberine (BBR) was administered at three different doses of 75, 150 and 300 mg/kg. A 60% alcohol was employed. The alcohol was administered at dose of 0.15 ml/10g body weight. The arrows indicate congestive necrosis places. (A): Observation of stomach and small intestines. Intestinal congestion occurs in the duodenum in model mouse. (B): Morphology of small intestines after alcohol administration. In the mouse model, small intestinal mucosa appears necrosis. BBR could prevent alcohol injury from the intestines. (C): Morphology of stomach after alcohol exposure. (D): Mucosa of small intestines (magnified 200 times). Alcohol causes gastric mucosal injury, edema with light staining. (E): Statistical score of the histopathological diagnoses for small intestines injury after alcohol consumption. Kruskal-Wallis chi-squared = 24.0696, df = 4, P = 7.735e-05. Data are expressed as the mean ± S.D. from six different mice. ###, vs. normal mice, P < 0.001. **, vs. model mice, P < 0.01.
Mentions: Two hours after 60% alcohol administration, the alcohol-induced pathological damage was observed as a congestive and dark red appearance in the duodenum compared with that of normal mice. High-dose BBR (300mg/kg) effectively inhibited the alcohol-induced morphological changes of the duodenum (Fig 1A). By light microscopy, congestion, edema, necrosis and shedding of the mucosa from duodenum was observed in alcohol-treated mice (Fig 1B and 1D). BBR was able to effectively antagonize the alcohol-induced pathological changes in the duodenum, which was indistinguishable in morphology from the saline group. Unlike the small intestine, the gastric mucosa exhibited minor pathological changes among the different groups (Fig 1C). It has previously been reported that 100% alcohol can cause erosion in rat stomach mucosa and can up-regulate the mRNA expression of c-fos, c-jun and HSP70 in the damaged epithelium; however, the necrosis in the stomach was less severe than in the small intestine[27], suggesting that the small intestines were more sensitive to alcohol damage.

Bottom Line: The purpose of the present study is to confirm the protective effect of berberine (BBR) on gastrointestinal injury caused by acute heavy alcohol exposure, an effect that has not been reported previously.Acute high alcohol concentrations lead to obvious damage to the gastrointestinal mucosa, resulting in necrosis of the intestinal mucosa.Oral administration of BBR was able to significantly reduce this alcohol-induced damage, inhibit increases of alcohol-induced TNFα and IL-1β expression in gastrointestinal mucosa as well as their upstream signals TLR2 and TLR4, and regulate cytokines that modulate tight junctions.

View Article: PubMed Central - PubMed

Affiliation: MOE Key Laboratory of Protein Sciences, Laboratory of Molecular Pharmacology and Pharmaceutical Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China.

ABSTRACT
The purpose of the present study is to confirm the protective effect of berberine (BBR) on gastrointestinal injury caused by acute heavy alcohol exposure, an effect that has not been reported previously. Our research details how BBR protects against gastrointestinal injuries from acute alcohol exposure using both in vivo and in vitro experiments. Acute high alcohol concentrations lead to obvious damage to the gastrointestinal mucosa, resulting in necrosis of the intestinal mucosa. Oral administration of BBR was able to significantly reduce this alcohol-induced damage, inhibit increases of alcohol-induced TNFα and IL-1β expression in gastrointestinal mucosa as well as their upstream signals TLR2 and TLR4, and regulate cytokines that modulate tight junctions. Alcohol consumption is a popular human social behavior worldwide, and the present study reports a comprehensive mechanism by which BBR protects against gastrointestinal injuries from alcohol stress, providing people with a novel application of BBR.

No MeSH data available.


Related in: MedlinePlus