## 1 Introduction  
Ulcerative colitis is the prolonged inflammation of the epithelial tissue of the colon with common symptoms such as diarrhoea, weight loss, abdominal pain, and rectal bleeding [1]. UC is three times more common in European and American populations than in Asian populations [2]. Despite the developed therapeutic options currently available, chronic inflammation of the colon can lead to bowel surgery or cancer risk. The major challenge in inflammatory bowel disease (IBD) research is the complex and poorly understood nature of the disease, that may be caused by a combination of environmental, genetic, and immune system factors. Additionally, these heterogeneity of IBD patient populations and the difficulty in accurately diagnosing and monitoring the disease also pose significant challenges in IBD research. All of the molecular events involved in the pathology of ulcerative colitis are complex and are a combination of changes in genetic, microbial, and other unknown factors. The hereditary component was confirmed by the observation that a higher percentage of IBDpatients have a family history of IBD [3]. The incidence was greater in the population of children of mothers with IBD. This indicates that maternal inheritance factors dominate ulcerative colitis-related genetic risk [4]. This same meta-analysis study also confirmed the 47 rick loci in ulcerative colitis [4]. Another major component of ulcerative colitis is lifestyle and environmental factors. Late-stage protection against ulcerative colitis is linked with early-life exposure to microbes. This is in sync with the positive correlation between better sanitation in developed countries and a lower incidence of ulcerative colitis [5]. Although the exact cause of the disease has not been determined, it is believed that overexpression of inflammatory markers such as TNF-, interferons, and interleukins cause upregulation of nuclear factor kappa beta sub-proteins [6; 7]. These overexpressed inflammatory cytokines and NF-kB cause weight loss, diarrhoea, bleeding, epithelial distortion, cryptic abscess, and damage to the mucosal layer of the colon in ulcerative colitis [8; 9; 10]. Therefore, research scientists are working on different synthetic and natural nano-formulations to inhibit the over-activation of NF-kB sub-molecules to cure ulcerative colitis. Conducting human studies is not possible for academic researchers and access to human tissue samples is a huge challenge. Thus, researchers are dependent on in vitro and in vivo models for laboratory-scale research and drug testing. There are several in vitro models of ulcerative colitis that are commonly used for research purposes:  
* Organoid culture: This involves the growth of colonic crypts in vitro to generate 3D structures that mimic the native tissue architecture [11]. * Cell line models: These models use immortalized cell lines such as Caco-2 or HT-29 cells, which are commonly used to study epithelial cell biology and inflammation [12]. * Co-culture models: These models use combinations of different cell types, such as epithelial cells and immune cells, to study interactions and inflammation in a more complex environment [13]. * Microfluidic models: These models utilise microfluidic devices to create controlled microenvironments for the study of cellular responses in a controlled and reproducible manner [14]. * Tissue-engineered models: These models utilise scaffolds or hydrogels to engineer 3D tissue structures that can be used to study various aspects of ulcerative colitis [15; 16]. Each of these models has its own advantages and limitations, and researchers can choose the most appropriate model based on the specific research question they are trying to answer. The major disadvantage of in-vitro models of IBD is reproducibility and lack of microbiota which is a key characteristic in the development of intestinal inflammation [17; 18; 19]. Hence, researchers heavily depend on in vivo models to conduct studies related to IBD research.