Evidence map›Paper›PMID 32248515›Full record

ArticleChinese journal of integrative medicine2021

Tojapride Reverses Esophageal Epithelial Inflammatory Responses on Reflux Esophagitis Model Rats.

Xiao-Lan Yin, Linda Zhong, Cheng-Yuan Lin, Xiao-Shuang Shi, Jiao Zhang, Zheng-Yi Chen, Hui Che, Xiang-Xue Ma, Ya-Xin Tian, Yuan-Zhi Duan and 5 more

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In one paragraph

Article in Chinese journal of integrative medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Xiao-Lan YinDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Linda ZhongSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong Special Administrative Region, Kowloon, China.
Cheng-Yuan LinSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong Special Administrative Region, Kowloon, China.
Xiao-Shuang ShiDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Jiao ZhangDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Zheng-Yi ChenDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Hui CheDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Xiang-Xue MaDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Ya-Xin TianDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Yuan-Zhi DuanDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Lin LuDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Hai-Jie JiDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Ying-Pan ZhaoCenter of Clinical Pharmacology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Xu-Dong TangDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Feng-Yun WangDepartment of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China. wfy811@163.com.
Xiyuan Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNHong Kong Baptist University · HKBeijing Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the mechanism of Tojapride, a Chinese herbal formula extract, on strengthening the barrier function of esophageal epithelium in rats with reflux esophagitis (RE).

methodsTen out of 85 SD rats were randomly selected as the sham group (n10), and 75 rats were developed a reflux esophagitis model (RE) by the esophageal and duodenal side-to-side anastomosis. Fifty successful modeling rats were divided into different medicated groups through a random number table including the model, low-, medium-, and high-dose of Tojapride as well as omeprazole groups (n10). Three doses of Tojapride [5.73, 11.46, 22.92 g/(kg•d)] and omeprazole [4.17 mg/(kg•d)] were administrated intragastrically twice daily for 3 weeks. And the rats in the sham and model groups were administered 10 mL/kg distilled water. Gastric fluid was collected and the supernatant was kept to measure for volume, pH value and acidity. Esophageal tissues were isolated to monitor the morphological changes through hematoxylin-eosin (HE) staining, and esophageal epithelial ultrastructure was observed by transmission electron microscopy. The expressions of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-KBp65), κB kinase beta (IKKß), occludin, and zonula occludens-1 (ZO-1) in the esophageal tissues were measured by immunohistochemistry and Western blot, respectively.

resultsThe gastric pH value in the model group was significantly lower than the sham group (P<0.05). Compared with the model group, gastric pH value in the omeprazole and medium-dose of Tojapride groups were significantly higher (P<0.05). A large area of ulceration was found on the esophageal mucosa from the model rats, while varying degrees of congestion and partially visible erosion was observed in the remaining groups. Remarkable increase in cell gap width and decrease in desmosome count was seen in RE rats and the effect was reversed by Tojapride treatment. Compared with the sham group, the IKKß levels were significantly higher in the model group (P<0.05). However, the IKKß levels were down-regulated after treatment by all doses of Tojapride (P<0.01 or P<0.05). The occluding and ZO-1 levels decreased in the model group compared with the sham group (Ps0.01 or Ps0.05), while both indices were significantly up-regulated in the Tojapride-treated groups (P<0.01 or P<0.05).

conclusionsTojapride could improve the pathological conditions of esophageal epithelium in RE rats. The underlying mechanisms may involve in down-regulating the IKKß expression and elevating ZO-1 and occludin expression, thereby alleviating the inflammation of the esophagus and strengthening the barrier function of the esophageal epithelium.

Indexed as

Esophagitis, PepticAnimalsDrugs, Chinese HerbalOccludinRatsRats, Sprague-DawleyDrugs, Chinese HerbalOccludinanti-inflammatoryesophageal epithelial barrierreflux-esophagitistojapride

Identifiers

PMID32248515
OpenAlexW3014645452

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.