Rat Endometriosis Model
Rat Endometriosis Model - Related Videos
08:02
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
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Cited by 62 •
2012
A description of the surgical induction of endometriosis in mice and rats by auto-transplantation of uterine tissue to the arterial cascade of the intestinal mesentery.
07:20
Intraoperative Detection of Subtle Endometriosis: A Novel Paradigm for Detection and Treatment of Pelvic Pain Associated with the Loss of Peritoneal Integrity
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Cited by 21 •
2012
Loss of peritoneal integrity provides a new paradigm to understand and treat chronic pelvic pain in women with mild forms of endometriosis and can be easily detected using intraoperative instillation of dye at the time of laparoscopy.
07:12
A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice
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Cited by 2 •
2020
Many rodent models of endometriosis are limited by technical complexity, reproducibility, and/or need for immunocompromised animals or special reporter mice. We present a simplified system of lesion induction using any experimental mouse with an independently verifiable, objective scoring system and with no requirement for ovariectomy or survival surgery.
08:16
Noninvasive Monitoring of Lesion Size in a Heterologous Mouse Model of Endometriosis
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Cited by 10 •
2019
Here, we present a protocol for live-imaging of fluorescently labeled human endometrial fragments grafted in mice. The method allows studying the effects of drugs of choice on endometriotic lesion size through monitoring and quantification of fluorescence emitted by the fluorescent reporter on real...
09:39
Creation of Reversible Cholestatic Rat Model
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2011
Cholestasis is a clinical condition commonly encountered by both surgeons and gastroenterologists. Creation of a reversible cholestatic rat model can be challenging in view of the smaller size and unique hepatopancreatobiliary anatomy in rats. This video article demonstrates the creation of a reversible cholestatic model.
FAQs
Hormonal cycling helps transferred endometrial tissue remain implanted and develop into lesions within the peritoneal cavity. This creates a setting in which ectopic tissue interacts with surrounding immune cells and promotes local inflammation. The resulting cytokine production provides measurable molecular signals for examining how immune activation supports lesion persistence and disease-related changes.
Altered macrophage and lymphocyte responses are important readouts because they show how the immune system reacts to ectopic endometrial-like tissue. In the rat model, researchers can examine these cell populations alongside lesion development and cytokine production. This connects cellular immune behavior with the inflammatory environment relevant to reproductive immunology.
Cytokine production helps link lesion biology to symptoms and progression. Within this model, local inflammatory signaling can be studied in relation to the growth of ectopic lesions and mechanisms of pelvic pain. Measuring these responses allows investigators to ask whether a treatment changes inflammatory activity, lesion development, or both.
To establish the model, researchers transfer uterine endometrial tissue into the rat’s peritoneal cavity and then examine the resulting ectopic growth under hormonal cycling. This workflow recreates the tissue placement and physiological context needed for lesion formation. It also provides a controlled experimental system for relating lesion development to immune-cell recruitment and inflammatory signaling.
Anti-inflammatory and immune-modulating therapies can be assessed by observing whether they alter lesion development, cytokine production, or immune-cell responses. Because the model links ectopic tissue with measurable inflammatory and cellular outcomes, it supports comparisons between treatment effects on disease mechanisms and effects on the lesions themselves. This makes it useful for translational reproductive-immunology research.
Results from the model can be interpreted across several levels: lesion growth, local cytokine production, immune-cell recruitment, and altered macrophage or lymphocyte responses. Considering these outcomes together is important because a therapy may affect inflammation without producing the same effect on lesions, or may reveal a mechanism connected to pelvic pain.