Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a chronic intestinal condition characterized by anemia, abdominal pain, diarrhea, and weight loss. The incidence of IBD has increased exponentially in the last decade, placing a significant financial burden on public health systems worldwide. Many factors can contribute to this disease, including genetic mutations, immune dysfunction, mucosal barrier defects, and intestinal flora disorders. Despite recent research on the mechanisms of IBD, including immune-, inflammatory-, and microbiome-related changes, the exact cause of IBD has not been determined. Interestingly, IBD is more prevalent in developing countries than in developed countries. The incidence of IBD in Asia has also increased significantly in recent years as a result of dietary changes [1], [2], [3]. With the increasing prevalence of inflammatory bowel disease, the threat to human health has become increasingly serious, and curing inflammatory bowel disease has become an important area of medical research. Currently, clinical treatment consists primarily of aminosalicylic acid preparation, hormone therapy, immunosuppressive therapy, fecal bacteria transplantation, monoclonal antibody therapy, and surgical therapy. The prognosis for patients with IBD is poor, and the side effects of these medications are more severe. At present, it is essential to explore the treatment of IBD in depth and to develop new treatment strategies [4].
There is still uncertainty concerning the etiology and pathogenesis of IBD. However, RONS are produced at sites of inflammation in the colon. Humans and laboratory animals have been shown to suffer from inflammatory bowel disease triggered by excessive levels of ROS/reactive nitrogen species (RNS) and the subsequent effects of oxidative stress and redox regulation. The role of ROS/RNS (superoxide anion (O2−•) and nitric oxide (NO)) in the progression of colitis is becoming increasingly evident [5,6]. ROS act as both signaling molecules and inflammatory mediators. Several animal and clinical studies have demonstrated that high levels of ROS can damage proteins, lipids, and DNA, thus resulting in intestinal inflammation, mucosal ulcers, and mucosal damage in the pathogenesis of IBD [7,8]. NO can mediate the pathological effects of tumor necrosis factor (TNF-α), interleukin-6 (IL-6) and other cytokines, leading to tissue damage and inflammation. Excess NO can damage the intestinal mucosa and epithelial barrier, inhibit intestinal movement, and cause intestinal inflammation [9,10]. In contrast, endogenous antioxidants are insufficient to eliminate excess ROS, so exogenous antioxidants are required to reduce excess ROS and maintain oxygen balance in the body, this is commonly known as antioxidant therapy. Antioxidant therapy is currently considered one of the most promising therapeutic options for treating and preventing a number of oxidative stress-related diseases [8,11].
Tannic acid (TA) is a natural polyphenol found in many herbs, such as black tea, green tea, and rhubarb, and has been shown to be beneficial in the treatment of acute and chronic intestinal inflammation. TA can be used for treating gastroenteritis and acute diarrhea [12], [13], [14]. TA may also precipitate proteins in the mucosa, forming a thin layer that protects it from inflammatory damage [15]. The anti-inflammatory properties of TA include its ability to scavenge free radicals and inhibit inflammatory mediators such as cytokines, nitric oxide synthase (iNOS) and inducible cyclooxygenase-2 (COX-2) [16], [17], [18]. Zinc (Zn) is an essential trace element in the body, and zinc deficiencies are associated with immune disorders as well as neurophysiological disorders [19,20]. Zinc deficiency can also result in intracellular oxidative stress, causing cellular dysfunction, and zinc plays a critical role in maintaining intracellular redox homeostasis [21,22]. IBD is characterized by an imbalance of free radicals. Zinc supplementation can reduce intestinal permeability and reverse IBD-related risks. Li Jinqua's research group has demonstrated that ZnO nanoparticles can release Zn2+ continuously and stably, effectively preventing IBD progression. The effects of ZnO NPs on inflammatory bowel disease are dose dependent, and they can significantly reduce colon shortening and pathological injury [23,24]. Riham Abdel-Hamid Haroun's research group reported that zinc nanoparticles coated with boswellic acid (BAs-ZnNPs) have good therapeutic efficacy against inflammatory bowel disease. The potential mechanisms of BAs-ZnNPs in the treatment of IBD include the inhibition of IL-8, IL-1β, IgG, IgM and ALP levels by regulating the expression of the PI3K and STAT-3 proteins and the COX-2 and NF-κB genes in UC rat models [25].
In this work, zinc ions were combined with tannic acids to form HZn-TA nanoparticles. HZn-TA nanoparticles were synthesized using a template composed of zeolitic imidazolate framework 8 (ZIF-8). In the first step, ZIF-8 nanoparticles were synthesized by a one-pot method [26]. On this basis, HZn-TA nanoparticles were etched by TA, and a multifunctional nanozyme. was developed for the treatment of IBD [27]. HZn-TA nanoparticles were shown to have good biocompatibility and RONS removal capabilities (Scheme 1). These factors are beneficial in the treatment and remission of inflammatory bowel disease. HZn-TA nanoparticles exhibit broad-spectrum free radical scavenging capabilities, including the ability to scavenge O2−• and NO. At the cellular level, several RONS, including superoxide anion (O2-•) and nitric oxide (NO), can be eliminated to increase cell survival following H2O2 stimulation. In a model for preventing and delaying acute colitis, clearance of RONS has been shown to reduce intestinal inflammation in mice by reducing colon damage, proinflammatory cytokine levels, the spleen index, and regaining body weight. HZn-TA nanoparticles promoted intestinal mucosal healing by upregulating ZO-1 and claudin-1 expression. According to the findings of this study, the use of zinc ions and tannic acid in the development of antioxidant nanoparticles could provide an attractive treatment option for IBD.
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