A compound plant extract for the prevention and treatment of colitis

Abstract

This invention relates to the field of biomedicine, specifically to a compound plant extract for the prevention and treatment of colitis. The compound plant extract of this invention is composed of oryzanol, octacosanol, curcumin, tea polyphenols, dihydromyricetin, and quercetin. This invention can simultaneously intervene in colitis at three key levels: anti-inflammation, anti-oxidation, and protection of the intestinal mucosal barrier. In a DSS-induced mouse colitis model, the compound plant extract of this invention significantly improved clinical symptoms such as weight loss, hematochezia, and diarrhea. Colonic histopathological examination showed a significant reduction in inflammatory response and effective protection of the mucosal structure. It is suitable for the treatment of inflammatory bowel diseases such as ulcerative colitis and Crohn's disease, with better efficacy than single-component formulations and higher safety, demonstrating good potential for clinical translation.

Description

Technical Field

[0001] This invention relates to the field of biomedicine, specifically to a compound plant extract for the prevention and treatment of colitis. Background Technology

[0002] Colitis is a type of inflammatory bowel disease characterized by chronic, nonspecific inflammation of the colonic mucosa, mainly including ulcerative colitis and Crohn's disease. Its clinical manifestations are typically abdominal pain, diarrhea, and bloody, mucus-containing stools. The condition often recurs and is difficult to cure, severely reducing patients' quality of life. Furthermore, long-term chronic inflammation can significantly increase the risk of colorectal cancer.

[0003] The pathogenesis of colitis is extremely complex, currently believed to be caused by the interaction of multiple factors, including genetic susceptibility, gut microbiota dysbiosis, intestinal mucosal barrier dysfunction, and immune response disorders. Within this pathological network, the following three links are consistently present and mutually reinforcing, forming a vicious cycle: First, there is the sustained activation of the immune inflammatory response. Abnormal activation of intestinal immune cells leads to the release of large amounts of pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6, forming a cytokine storm that directly damages intestinal epithelial cells and recruits more inflammatory cells to infiltrate, resulting in persistent tissue damage. Second, there is a significant exacerbation of oxidative stress damage. Under inflammatory conditions, reactive oxygen species accumulate in large quantities, exceeding the clearance capacity of the endogenous antioxidant system, attacking cell membrane lipids, proteins, and nucleic acids, and disrupting the structural integrity and function of intestinal epithelial cells. Third, there is the disruption of the structure and function of the intestinal mucosal barrier. Pro-inflammatory cytokines and oxidative stress together lead to the downregulation of tight junction proteins in the intestinal epithelium, significantly increasing intestinal permeability, allowing antigens in the intestinal lumen to translocate into the deep intestinal wall, and continuously driving abnormal immune responses.

[0004] The three links mentioned above are mutually causal and exacerbate each other: inflammation drives oxidative stress, oxidative stress exacerbates inflammation and barrier damage, and barrier damage leads to more antigens entering the mucosa, triggering a stronger immune response. This vicious cycle means that intervention targeting only one link is unlikely to effectively halt disease progression. Therefore, developing treatment plans that can simultaneously act on the three key links of anti-inflammation, anti-oxidation, and intestinal barrier protection, achieving multi-target synergistic intervention, is of great significance for improving the clinical efficacy of colitis treatment. Summary of the Invention

[0005] The purpose of this invention is to provide a compound plant extract for the prevention and treatment of colitis, in order to solve the problem that existing single-component drugs have limited anti-inflammatory effects and are difficult to achieve synergistic intervention on inflammation, oxidative stress and intestinal barrier damage.

[0006] To achieve the above objectives, the present invention adopts the following technical solution: a compound plant extract, wherein the compound plant extract is composed of the following components in parts by weight: 180-220 parts of oryzanol, 180-220 parts of octacosanol, 180-220 parts of curcumin, 80-120 parts of tea polyphenols, 180-220 parts of dihydromyricetin, and 80-120 parts of quercetin.

[0007] Furthermore, the compound plant extract is composed of the following components in parts by weight: 200 parts of oryzanol, 200 parts of octacosanol, 200 parts of curcumin, 100 parts of tea polyphenols, 200 parts of dihydromyricetin, and 100 parts of quercetin.

[0008] A pharmaceutical preparation comprising the compound plant extract as described in any one of claims 1-2, and a carrier and / or excipients.

[0009] Furthermore, the carrier includes water.

[0010] Furthermore, the excipients include Eudragit S100.

[0011] The application of the above-mentioned compound plant extracts in the prevention and / or treatment of colitis.

[0012] Furthermore, the colitis mentioned includes ulcerative colitis or Crohn's disease.

[0013] Furthermore, the compound plant extract is an oral preparation.

[0014] Furthermore, the oral formulation includes tablets, capsules, granules, or oral liquids.

[0015] The beneficial effects of this invention are: 1. In a DSS-induced mouse colitis model, after administration of the compound plant extract of this invention (2 g / kg) for 9 days, the DAI score decreased by 4.2 compared with the model group. More importantly, the DAI score and histological score of this compound group were significantly lower (p < 0.05) than those of the single-use groups of oryzanol, octacosanol, curcumin, tea polyphenols, dihydromyricetin, and quercetin, as well as the control group of any combination thereof, demonstrating a synergistic effect.

[0016] 2. Mechanistic studies have shown that the composition of the present invention can simultaneously and significantly reduce the protein and mRNA levels of TNF-α, IL-6, and IL-1β in colonic tissue; significantly increase the activity of superoxide dismutase and glutathione peroxidase in the tissue, reduce malondialdehyde content; and significantly upregulate the expression of tight junction proteins Occludin and ZO-1; thus achieving integrated treatment with anti-inflammatory, antioxidant, and intestinal barrier protection effects.

[0017] 3. All components of this invention are natural plant extracts or natural equivalents, which are highly safe; the preparation process of the composition is simple, involving only physical mixing, without the need for complex synthesis or extraction steps, and is inexpensive, which is conducive to industrialization and clinical application. Attached Figure Description

[0018] Figure 1 These are images showing the bleeding patterns of mice in each experimental group of this invention; Figure 2 This is a graph showing the changes in body weight of mice in each experimental group of this invention (*: p <0.05; **: p <0.01); Figure 3 This is a DAI score chart of mice in each experimental group of this invention (*: p <0.05; **: p <0.01); Figure 4 This is a diagram showing the effects of each experimental group of this invention on the colorectal region of mice (*: p <0.05; **: p <0.01); (A) Representative colorectal diagrams under different treatments; (B) Colorectal length measurement diagram; Figure 5 The following are graphs showing the effects of different experimental groups of this invention on the spleen of mice (*: p < 0.05; **: p < 0.01): (A) Representative spleen graphs under different treatments; (B) Spleen index graph. Figure 6 These are histopathological changes in the colon tissue of mice in each experimental group of this invention; Figure 7 This is a graph showing the effect of each experimental group of the present invention on the expression level of inflammatory factor proteins in mouse colon tissue (*: p < 0.05; **: p < 0.01). Figure 8 This is a graph showing the effect of each experimental group of the present invention on the expression level of intestinal barrier protein in mouse colon tissue (*: p < 0.05; **: p < 0.01). Detailed Implementation

[0019] The technical solution of the present invention will now be clearly and completely described with reference to the accompanying drawings in the embodiments of the present invention.

[0020] This invention combines oryzanol, octacosanol, curcumin, tea polyphenols, dihydromyricetin and quercetin in specific proportions to produce a significant synergistic effect.

[0021] This synergistic effect is specifically manifested in the following ways: 1. Synergistic complementarity of anti-inflammatory pathways Curcumin and tea polyphenols mainly reduce the production of pro-inflammatory factors such as TNF-α and IL-6 by inhibiting the NF-κB signaling pathway; while dihydromyricetin and quercetin tend to activate the Nrf2 / ARE antioxidant pathway and regulate the gut microbiota; the combination of the two blocks the cytokine storm both upstream and downstream.

[0022] 2. Three-dimensional construction of antioxidant networks Tea polyphenols, dihydromyricetin, and quercetin are all potent antioxidants, but they each have their own focus in terms of intracellular and extracellular distribution and free radical scavenging spectrum. The combination of these three forms a three-dimensional antioxidant network extending from the extracellular to the intracellular and from the aqueous to the lipid phase. This invention reveals that the presence of oryzanol and octacosanol can stabilize this network and enhance its activity.

[0023] 3. Comprehensive strengthening of intestinal barrier protection Oryzanol and octacosanol have been shown to upregulate the expression of tight junction proteins (such as Occludin and ZO-1) and repair intestinal epithelial spaces. This, combined with the inhibitory effects of curcumin and quercetin on matrix metalloproteinases and their protective effects on intestinal epithelial cells, comprehensively strengthens the intestinal mucosal barrier at both structural and cellular levels. Based on a deep understanding of the aforementioned synergistic mechanism, this invention, through extensive optimization experiments, ultimately determined the optimal ratio range.

[0024] The DSS-induced mouse colitis model experiment confirmed that the compound plant extract with this specific ratio was significantly better than any single component or any combination of two or three components in reducing DAI scores, inhibiting the levels of pro-inflammatory factors (TNF-α, IL-6, IL-1β), and alleviating pathological damage to colon tissue. The high-dose group was comparable to the positive drug group, demonstrating positive and beneficial technical effects.

[0025] Example 1 This embodiment evaluates the preparation method and efficacy of the compound plant extract described in this invention.

[0026] I. Preparation of the compound of this invention Weigh out the active ingredients (total 1000 mg) according to the following ratio: 200 mg oryzanol, 200 mg octacosanol, 200 mg curcumin, 100 mg tea polyphenols, 200 mg dihydromyricetin, and 100 mg quercetin. Mix the above ingredients evenly and dissolve them in sterile water to prepare a compound turbid solution for later use.

[0027] II. Laboratory Animals and Grouping Fifty male SPF-grade ICR mice, aged 6-7 weeks and weighing 20-25g, were selected. The animal room was set up with a 12h light / 12h dark cycle, a temperature of 22-25℃, and a relative humidity of 55%-77%.

[0028] After 7 days of acclimatization, the mice were randomly divided into 5 groups of 10 mice each: normal control group (CON), model group (DSS), low-dose compound group (DSS + compound 100, 100 mg / kg / d), high-dose compound group (DSS + compound 200, 200 mg / kg / d) and positive control group (5-aminosalicylic acid, 50 mg / kg / d).

[0029] III. Establishment of the Colitis Model and Drug Administration Regimen Mice in the CON group drank purified water continuously during the experiment; mice in the DSS group, DSS+compound 100 group, DSS+compound 200 group and positive control group drank purified water on days 1-2 of the experiment, and drank 3.0% (w / v) sodium dextran sulfate (DSS) aqueous solution on days 3-9.

[0030] The low-dose and high-dose compound groups were administered compound solution by gavage at 100 mg / kg and 200 mg / kg respectively on days 1 to 9 of the experiment. The positive control group was administered 5-aminosalicylic acid (50 mg / kg) by gavage. The CON group and DSS group were administered the same volume of purified water by gavage. All groups were administered the drug continuously for 9 days, at a fixed time every morning.

[0031] The DSS concentration and treatment time used in this experiment were determined based on previous research results. After the experiment, the mice were euthanized by cervical dislocation, and the colon, spleen and other tissues were separated. After recording the length of the colon and the weight of the spleen, the tissues were stored in an ultra-low temperature freezer at -80℃.

[0032] IV. Macroscopic Phenotypic Observation Observe the mice daily for general conditions such as mental state, activity level, and fur luster, record weight, fecal characteristics and blood in stool, and calculate the disease activity index (DAI).

[0033] like Figure 1 As shown, mice in the DSS group had obvious bleeding marks, while the bleeding degree in both the low- and high-dose compound groups was significantly reduced, and the improvement was more obvious in the high-dose group.

[0034] Weight change is a key indicator for evaluating the success of the DSS-induced ulcerative colitis model; such as Figure 2 As shown, at the end of the experiment, the DSS group mice had a significantly lower body weight compared to the CON group. p <0.01); Although the body weight of both the low- and high-dose compound groups decreased, it was higher than that of the DSS group ( p<0.05), showing a dose-dependent effect. At the experimental endpoint, the body weight of the CON group was (36.81±1.94) g, an increase of 36.33% compared to the starting weight; the body weight of the DSS group was (28.47±1.61) g, an increase of 5.44% compared to the starting weight; the body weight of the low-dose compound group was (29.91±0.89) g, an increase of 10.78% compared to the starting weight; the body weight of the high-dose compound group was (34.46±0.58) g, an increase of 27.62% compared to the starting weight; and the body weight of the positive control group was (33.06±0.74) g, an increase of 22.44% compared to the starting weight.

[0035] It is evident that the weight loss trend in the compound pre-protective group was slower than that in the DSS group, and the high-dose group showed better recovery; in addition, the stools of mice in the DSS group were loose and unformed, and later, diarrhea, occult blood, and even bloody stools appeared; Figure 3 As shown, compared with the DSS group (DAI score of 9.3), the DAI scores of the low-dose and high-dose compound groups were 6.5 and 5.1, respectively, which were significantly lower. p <0.05), fecal occult blood and diarrhea scores decreased, symptoms were relieved, and the high-dose group showed better results. These results suggest that the compound of this invention has a dose-dependent alleviating effect on DSS-induced ulcerative colitis (UC) symptoms in mice.

[0036] V. Effects of the compound on the colon, rectum, and spleen of UC mice At the end of the experiment, the colon and rectum were completely dissected and their length was observed and measured. The results are as follows: Figure 4 As shown, the lengths of the colon and rectum in mice in the CON group, DSS group, low-dose compound group, and high-dose compound group were (9.11±0.94) cm, (5.13±1.04) cm, (6.35±0.78) cm, (6.74±1.10) cm, and (7.30±1.10) cm, respectively.

[0037] After drinking DSS water, the colon and rectum of mice were significantly shortened. The colon and rectum length in the DSS group decreased to 0.56 times that in the CON group (P<0.01). Compared with the DSS group, the colon and rectum length in the low-dose and high-dose compound groups increased by 23.52% (P<0.05) and 31.37% (P<0.01), respectively. The results indicate that the compound can alleviate DSS-induced colon and rectum shortening in a dose-dependent manner.

[0038] The spleen is an important immune organ in the body. Its size and shape affect the normal growth and physiological function of immune cells such as lymphocytes, and can reflect the body's immune level. DSS stimulation can induce UC and cause an immune response in mice, leading to splenomegaly.

[0039] After the experiment, the spleen tissue of the mice was observed and weighed. Considering the influence of body weight, the spleen index (spleen weight / body weight) was used for statistical analysis; for example... Figure 5 As shown, the differences in spleen size among the mice in each group are illustrated.

[0040] The spleen indices of mice in the CON group, DSS group, low- and high-dose compound group, and positive control group were 0.31±0.01, 0.42±0.02, 0.35±0.01, 0.34±0.01, and 0.33±0.02, respectively. Compared with the CON group, the spleen index of mice in the DSS-damaged group increased by 1.35 times (P<0.01). Compared with the DSS group, the spleen index of the low-dose compound group decreased by 16.66% (P<0.05), and the high-dose compound group decreased by 19.04% (P<0.01), with more significant recovery of spleen morphology in the high-dose group. These results suggest that the compound of this invention can reverse DSS-induced splenomegaly and abnormal immune response to a certain extent in a dose-dependent manner.

[0041] VI. Histopathological Analysis After the experiment, the mice were fasted for 12 hours and then sacrificed. The entire colon was quickly removed and its length was measured. The distal colon tissue was taken, fixed with 4% paraformaldehyde, dehydrated, embedded, sectioned, and stained with H&E. The pathological changes such as inflammatory cell infiltration, epithelial damage, crypt structure destruction, and submucosal edema were observed under a microscope.

[0042] The results showed that the compound of the present invention could significantly improve the symptoms of weight loss, diarrhea and bloody stools induced by DSS in mice, reduce inflammatory damage to colon tissue, and protect the integrity of intestinal mucosal structure. Moreover, the high-dose group was more effective than the low-dose group, which verified its good anti-colitis effect.

[0043] DSS-induced UC leads to phenotypes such as colonic shortening, edema, and ulceration in mice. Figure 6 As shown, this experiment analyzed colon tissue using H&E staining. Compared with the CON group, the DSS group showed disruption of colonic gland crypt structure and impaired mucosal barrier function; a significant reduction in goblet cells and decreased integrity of the mucus protective layer; and the presence of a large number of inflammatory cells such as lymphocytes and neutrophils, which exacerbated colon tissue damage and inflammatory response. Compared with the DSS group, the low- and high-dose compound groups showed relatively intact mucosal and crypt structures and significantly reduced inflammatory cell infiltration, with the high-dose group exhibiting a more significant repair effect. This suggests that the compound of this invention has the effect of protecting the colonic mucosal barrier and reducing inflammatory damage, and this effect is dose-dependent.

[0044] VII. The compound formula can downregulate the protein expression of pro-inflammatory cytokines in the colonic tissue of UC mice and upregulate the protein expression of anti-inflammatory molecules. IL-1β, IL-6, TNF-α, and IL-10 are cytokines with extensive inflammatory effects, and their abnormal expression is closely related to the severity of inflammation. The degree of inflammatory response can be assessed by detecting the levels of IL-1β, IL-6, TNF-α, and IL-10 in colon tissue. The results are shown in Table 1. Table 1. Comparison of cytokine levels in colonic tissue of DSS colitis model mice (mean ± SD, n=3)

[0045] Note: ** indicates comparison with the normal control group. P <0.01; ## indicates that compared with the DSS model group, P <0.01; # indicates that compared with the DSS model group, P <0.05.

[0046] Compared with the normal control group, the levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α in the colonic tissue of mice in the DSS model group were significantly increased (P < 0.01), rising from 37.94 pg / mg prot, 27.13 pg / mg prot, and 31.46 pg / mg prot to 163.87 pg / mg prot, 109.64 pg / mg prot, and 147.39 pg / mg prot, respectively; while the level of anti-inflammatory cytokine IL-10 was significantly decreased (P < 0.01), from 53.27 pg / mg prot to 14.86 pg / mg prot, indicating that the DSS-induced colitis model was successfully established and the colonic tissue showed a significant pro-inflammatory state; after intervention with the positive control drug (mesarazidine, 300 mg / kg / d), all the above indicators were significantly reversed.

[0047] Compared with the DSS model group, the levels of IL-1β, IL-6, and TNF-α in the colon tissue of mice in the positive drug group were significantly decreased (P < 0.01), decreasing to 61.48 pg / mg prot, 45.29 pg / mg prot, and 57.63 pg / mg prot, respectively; while the level of IL-10 significantly increased (P < 0.01), reaching 39.74 pg / mg prot, indicating that the positive drug effectively inhibited the inflammatory response in the colon; after administration of different doses of the compound, a significant dose-dependent improvement effect was observed.

[0048] In the low-dose group, the levels of IL-1β, IL-6, and TNF-α were 97.31 pg / mg prot, 73.86 pg / mg prot, and 83.51 pg / mg prot, respectively, all significantly lower than those in the DSS model group (P < 0.05). The IL-10 level (24.69 pg / mg prot) was significantly higher than that in the DSS model group (P < 0.05). The high-dose group showed even more significant effects, with further reductions in the levels of each pro-inflammatory factor (IL-1β: 54.69 pg / mg prot, IL-6: 41.37 pg / mg prot, TNF-α: 49.23 pg / mg prot) and a further increase in the IL-10 level to 43.18 pg / mg prot, comparable to the positive control group (no statistical difference between groups, P > 0.05), and significantly better than the low-dose group (P < 0.05 or P < 0.01). The above results indicate that the relapsed drug can alleviate DSS-induced inflammatory response in colonic tissue in a dose-dependent manner, and the anti-inflammatory effect of the high-dose group is similar to that of the positive control drug.

[0049] like Figure 7 The figure shows the relative expression levels (mRNA) of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and anti-inflammatory cytokines (IL-10) in the colon tissue of the DSS model group. Compared with the normal control group, the protein and mRNA levels of IL-1β, IL-6, and TNF-α were significantly increased, while the protein and mRNA levels of IL-10 were significantly decreased (P < 0.01). After intervention with the positive control drug and different doses of the test drug, the above indicators showed a dose-dependent reversal, with the high-dose group showing an effect comparable to the positive control drug group. The trends of protein and mRNA results were consistent, indicating that the test drug could effectively inhibit DSS-induced colonic inflammation at both the transcriptional and translational levels.

[0050] 8. The upregulation effect of the compound on the expression of tight junction protein in the colon tissue of UC mice The intestinal barrier, as the body's main line of defense for regulating intestinal bacteria and clearing antigens, is crucial for maintaining intestinal homeostasis. To evaluate the effect of the compound on the repair of intestinal barrier integrity in colitis mice, this study further examined the mRNA and protein expression levels of the tight junction proteins Occludin and Claudin-1 in colon tissue.

[0051] like Figure 8As shown, compared with the normal control group (CON), the mRNA and protein expression levels of Occludin and Claudin-1 in the colon tissue of DSS model mice were significantly reduced (both P < 0.01), indicating that the intestinal barrier structure of DSS-induced colitis model mice was severely damaged and the intestinal epithelial permeability was significantly increased. Compared with the DSS model group, the compound treatment groups (100, 200 mg / kg) significantly upregulated the mRNA and protein expression of Occludin and Claudin-1 in a dose-dependent manner: the low-dose compound group (DSS + compound 100) could partially restore the expression levels of the two tight junction proteins (P < 0.05 or P < 0.01); the high-dose compound group (DSS + compound 200) showed a more significant repair effect (both P < 0.01), and its regulatory level on tight junction proteins was not significantly different from that of the positive drug group (P > 0.05), suggesting that the compound can effectively repair the damaged intestinal barrier function of colitis mice, and the repair effect of the high-dose compound is comparable to that of the positive drug.

[0052] In summary, the compound formula of this invention can improve the pathological process of DSS-induced colitis through a dual mechanism: on the one hand, it reduces intestinal inflammatory damage by inhibiting the excessive release of pro-inflammatory factors and restoring the level of anti-inflammatory factors; on the other hand, it repairs the damaged intestinal barrier structure and reduces the infiltration and spread of inflammatory factors by upregulating the expression of tight junction proteins Occludin and Claudin-1. Furthermore, all of the above effects show a clear dose-dependent relationship, and the anti-inflammatory and barrier repair effects of high-dose compound formula are not significantly different from those of positive control drugs, providing experimental evidence for the application of the compound formula in the treatment of colitis.

[0053] Comparative Example 1 To verify the synergistic effect of the composition of the present invention, we set up a complete comparative experiment.

[0054] In addition to the groups described in Example 1 (normal group, model group, compound group, and positive control group), six single-component groups were added (each administered 200 mg / kg of oryzanol, octacosanol, curcumin, and dihydromyricetin, and 100 mg / kg of tea polyphenols and quercetin, respectively) and multiple permutation and combination control groups, with the dosage corresponding to the dosage of each component in the compound. All experimental procedures, detection indicators, and evaluation methods were the same as in Example 1.

[0055] Experimental results: 1. Comparison of Disease Activity Indices At the experimental endpoint (day 9), the DAI in the model group was 9.3. The DAI in the compound administration group decreased to 5.1, showing a significant effect. Among the single-component groups, the curcumin group, which showed the best effect, only reduced its DAI to 7.8, while the DAI of other single-component groups ranged from 7.8 to 8.9. The DAI score of the compound group was significantly lower than that of all single-component groups (p < 0.01) and the control group of any component combination, demonstrating a significant synergistic improvement effect.

[0056] 2. Comparison of colonic histopathological scores The colonic mucosal epithelium of mice in the compound administration group was intact, with mild inflammatory cell infiltration and crypt damage. The histological score was significantly lower than that of the model group and was significantly better than all single-component groups.

[0057] 3. Comparison of inflammatory factor levels The protein and mRNA levels of TNF-α and IL-6 in the colon tissue of the compound-treated group were significantly inhibited, and the inhibitory effect was significantly stronger than the sum of the effects of any single component group. This directly confirms the existence of synergistic effect from the data.

[0058] The above comparative experiments conclusively prove that the specific combination of the six specific components claimed in this invention is not a simple accumulation of components, but rather produces a valuable and unexpected synergistic effect, which constitutes a solid foundation for the inventiveness of this invention.

[0059] This invention is not limited to the preferred embodiments described above. Anyone can derive other products in various forms under the guidance of this invention. However, regardless of any changes made in their shape or structure, any technical solution that is the same as or similar to this invention falls within the protection scope of this invention.

Claims

1. A compound plant extract, characterized in that, The compound plant extract is composed of the following components in parts by weight: 180-220 parts of oryzanol, 180-220 parts of octacosanol, 180-220 parts of curcumin, 80-120 parts of tea polyphenols, 180-220 parts of dihydromyricetin, and 80-120 parts of quercetin.

2. The compound plant extract according to claim 1, characterized in that, The compound plant extract is composed of the following components in parts by weight: 200 parts of oryzanol, 200 parts of octacosanol, 200 parts of curcumin, 100 parts of tea polyphenols, 200 parts of dihydromyricetin, and 100 parts of quercetin.

3. A pharmaceutical preparation, characterized in that: It comprises the compound plant extract as described in any one of claims 1-2, as well as a carrier and / or excipients.

4. The pharmaceutical preparation according to claim 3, characterized in that: The carrier includes water.

5. The pharmaceutical preparation according to claim 3, characterized in that: The excipients include Eudragit S100.

6. The use of the compound plant extract according to claim 1 or 2 in the prevention and / or treatment of colitis.

7. The application according to claim 6, characterized in that: The colitis mentioned includes ulcerative colitis or Crohn's disease.

8. The application according to claim 6, characterized in that: The compound plant extract is an oral preparation.

9. The application according to claim 8, characterized in that: The oral preparations include tablets, capsules, granules, or oral liquids.

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