Therapeutic Effect of Combining Anisodamine With Neostigmine on Local Scar Formation Following Roux-en-Y Choledochojejunostomy in a Novel Rat Model

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Abstract

Background: The present study aimed to explore the potential effect of combining anisodamine with neostigmine on local scar formation following Roux-en-Y choledochojejunostomy (RCJS) in a novel rat model.

Methods: The biliary obstruction model of Sprague Dawley (SD) rats was established in advance, and 54 rats were divided into nine groups randomly (sham operation group, anisodamine group, neostigmine group, combination group, and control group). Anisodamine (25 mg/kg) and neostigmine (50 μg/kg) were injected to the abdominal cavity separately or simultaneously for 1 week since the first day after surgery according to their allocated intervention, while the same amount of saline (0.5 ml) was injected intraperitoneally in the control group. Indexes including body weight, the diameter of the common bile duct, liver function, inflammatory indexes, and the condition of scar formation in different groups at certain time were evaluated in our study.

Results: Recovery of liver function (ALT, AST, TB, DB, and GGT) and systematic inflammation indexes (CRP, TNF-α, and IL-1β) in the combination group was prior to that in the control group ( p < 0.05), while no statistical difference in the serum level of IL-10 was observed among groups. Rats in the combination group represented a wider anastomotic diameter and lower expression of α-SMA and TGF-β1 at anastomotic stoma compared to the control group ( p < 0.05). Histopathological staining showed slighter proliferation of collagen and smooth muscle fibers in rats’ bile duct wall and less local scar formation at anastomotic stoma compared to the control group.

Conclusion: The combination of anisodamine and neostigmine can alleviate local and systemic inflammatory response, promote the recovery of liver function, and reduce scar formation in rats after the RCJS procedure.

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In post-natal life the inflammatory response is an inevitable consequence of tissue injury. Experimental studies established the dogma that inflammation is essential to the establishment of cutaneous homeostasis following injury, and in recent years information about specific subsets of inflammatory cell lineages and the cytokine network orchestrating inflammation associated with tissue repair has increased. Recently, this dogma has been challenged, and reports have raised questions on the validity of the essential prerequisite of inflammation for efficient tissue repair. Indeed, in experimental models of repair, inflammation has been shown to delay healing and to result in increased scarring. Furthermore, chronic inflammation, a hallmark of the non-healing wound, predisposes tissue to cancer development. Thus, a more detailed understanding in mechanisms controlling the inflammatory response during repair and how inflammation directs the outcome of the healing process will serve as a significant milestone in the therapy of pathological tissue repair. In this paper, we review cellular and molecular mechanisms controlling inflammation in cutaneous tissue repair and provide a rationale for targeting the inflammatory phase in order to modulate the outcome of the healing response.

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Damage to any tissue triggers a cascade of events that leads to rapid repair of the wound - if the tissue is skin, then repair involves re-epithelialization, formation of granulation tissue and contraction of underlying wound connective tissues. This concerted effort by the wounded cell layers is accompanied by, and might also be partially regulated by, a robust inflammatory response, in which first neutrophils and then macrophages and mast cells emigrate from nearby tissues and from the circulation. Clearly, this inflammatory response is crucial for fighting infection and must have been selected for during the course of evolution so that tissue damage did not inevitably lead to death through septicemia. But, aside from this role, exactly what are the functions of the various leukocyte lineages that are recruited with overlapping time courses to the wound site, and might they do more harm than good? Recent knockout and knockdown studies suggest that depletion of one or more of the inflammatory cell lineages can even enhance healing, and we discuss new views on how regulation of the migration of inflammatory cells to sites of tissue damage might guide therapeutic strategies for modulating the inflammatory response.

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Interrelation of immunity and tissue repair or regeneration.

Sabine A. Eming, Matthias Hammerschmidt, Thomas Krieg … (2009)

Although tremendous progress has been achieved in understanding the molecular basis of tissue repair and regeneration in diverse model organisms, the tendency of mammals for imperfect healing and scarring rather than regeneration remains unexplained. Moreover, conditions of impaired wound healing, e.g. non-healing skin ulcers associated with diabetes mellitus or vascular disease, as well as excessive scarring, represent major clinical and socio-economical problems. The development of innovative strategies to improve tissue repair and regeneration is therefore an important task that requires a more thorough understanding of the underlying molecular and cellular mechanisms. There is substantial evidence in different model organisms that the immune system is of primary importance in determining the quality of the repair response, including the extent of scarring, and the restoration of organ structure and function. Findings in diverse species support a correlation between the loss of regeneration capacity and maturation of immune competence. However, in recent years, there is increasing evidence on conditions where the immune response promotes repair and ensures local tissue protection. Hence, the relationship between repair and the immune response is complex and there is evidence for both negative and positive roles. We present an overview on recent evidence that highlights the immune system to be key to efficient repair or its failure. First, we summarize studies in different model systems that reveal both promoting and impeding roles of the immune system on the regeneration and repair capacity. This part is followed by a delineation of diverse inflammatory cell types, selected peptide growth factors and their receptors as well as signaling pathways controlling inflammation during tissue repair. Finally, we report on new mechanistic insights on how these inflammatory pathways impair healing under pathological conditions and discuss therapeutic implications.

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Author and article information

Contributors

Shao-cheng Lyu: URI : https://loop.frontiersin.org/people/1376205/overview

Jing Wang: URI : https://loop.frontiersin.org/people/1203682/overview

Journal

Journal ID (nlm-ta): Front Pharmacol

Journal ID (iso-abbrev): Front Pharmacol

Journal ID (publisher-id): Front. Pharmacol.

Title: Frontiers in Pharmacology

Publisher: Frontiers Media S.A.

ISSN (Electronic): 1663-9812

Publication date (Electronic): 29 September 2021

Publication date Collection: 2021

Volume: 12

Electronic Location Identifier: 700050

Affiliations

Department of Hepatobiliary and Pancreaticosplenic Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China

Author notes

Edited by: Pallavi R. Devchand, University of Calgary, Canada

Reviewed by: Yuanli Chen, Hefei University of Technology, China

Ling-shiang Felix Chuang, Icahn School of Medicine at Mount Sinai, United States

*Correspondence: Ren Lang, langren@ 123456bjcyh.com

[ † ]

These authors have contributed equally to this work

This article was submitted to Inflammation Pharmacology, a section of the journal Frontiers in Pharmacology

Article

Publisher ID: 700050

DOI: 10.3389/fphar.2021.700050

PMC ID: 8511430

PubMed ID: 34658849

SO-VID: e8b122af-4609-484e-81d1-87ff75e09975

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 25 April 2021

Date accepted : 14 June 2021

Funding

Funded by: Beijing Municipal Natural Science Foundation , doi 10.13039/501100005089;

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Therapeutic Effect of Combining Anisodamine With Neostigmine on Local Scar Formation Following Roux-en-Y Choledochojejunostomy in a Novel Rat Model

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Most cited references 35

Inflammation in wound repair: molecular and cellular mechanisms.

Inflammatory cells during wound repair: the good, the bad and the ugly.

Interrelation of immunity and tissue repair or regeneration.

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