Natural Products and Bioprospecting
·
2026
·Vol. 16
·期 1
·76
·
IF 5.8
Li Liang,Zhan Xinyi,Ullah Hidayat,Guo Wenxian,Gui Ping,Peng Weijie,Mei Quanxi,Dai Weibo,Duan Yuting,Yuan Xia,Hu Xianjing
Inflammatory bowel disease (IBD) is a chronic disorder characterized by recurrent intestinal inflammation and gut microbiota dysbiosis. Huanglian-Wendan Decoction (HLWDD) has been clinically used for IBD treatment; however, its underlying mechanisms remain unclear. In this study, a dextran sulfate sodium (DSS, 2.25%)-induced IBD mouse model was established to evaluate the therapeutic effects of HLWDD. The protective mechanisms were investigated in colon tissues of DSS-induced mice using ELISA, immunoblotting, histological, and immunohistochemical analyses. In addition, the impact of HLWDD on gut microbiota dysbiosis was analyzed using 16S rRNA sequencing. Antibiotic treatment was applied before DSS administration to deplete gut microbiota and verify the role of microbial modulation. Furthermore, the phytochemical constituents of HLWDD were characterized using liquid chromatography–quadrupole time-of-flight tandem mass spectrometry (LC-QTOF-MS/MS). The results demonstrated that HLWDD markedly alleviated DSS-induced colitis, as evidenced by reduced body weight loss, rectal bleeding, colon shortening, and disease activity index (DAI) scores. Mechanistically, HLWDD suppressed inflammatory responses in colon tissues by inhibiting the TLR4/MyD88/NF-κB and IL-6/JAK2/STAT3 signaling pathways, while enhancing epithelial barrier integrity through upregulation of ZO-1, Occludin, Claudin-1, and Mucin-2. In addition, HLWDD attenuated endoplasmic reticulum stress (ERS) and apoptosis by downregulating CHOP, phospho-eIF2α, cleaved caspase-3, and Bax, while increasing Bcl-2 expression in colonic tissues. Microbiota analysis revealed an increased abundance of beneficial bacterial genera such as Akkermansia and Escherichia-Shigella –related commensals, along with enrichment of beneficial bacterial families including Ruminococcaceae , Lachnospiraceae , and Verrucomicrobiaceae , whereas potentially harmful taxa such as Escherichia and Paraprevotella were reduced. HLWDD also increased the production of short-chain fatty acids (SCFAs), including acetate, butyrate, and isobutyrate, thereby promoting intestinal homeostasis. Importantly, the protective effects of HLWDD were largely abolished following antibiotic-mediated gut microbiota depletion, confirming the essential role of microbial modulation in its therapeutic action. Collectively, these findings suggest that HLWDD ameliorates IBD by regulating gut microbiota composition and function, thereby inhibiting colonic ER stress and apoptosis and restoring intestinal barrier integrity. This study provides mechanistic evidence supporting the potential clinical application of HLWDD as a novel therapeutic strategy for IBD. Graphical
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PHYTOTHERAPY RESEARCH
·
2026
·
IF 8.1
Bingyu Chen,Ke Liu,Yaya Guo,Jingwei Zhao,Yanhua Wang
The global incidence of ulcerative colitis (UC), a chronic inflammatory bowel disease, is rising. Epi-berberine (EPI), an alkaloid from Coptidis Rhizoma , shows potential for UC treatment. This study aimed to assess EPI's effect on UC and explore the mechanism underlying its UC-alleviating effect. The therapeutic effects of EPI on UC were validated in dextran sulfate sodium (DSS)-induced colitis mice and lipopolysaccharide (LPS)-induced Caco-2 inflammatory models and further investigated the underlying mechanism. In vivo, high-dose EPI (200 mg/kg) attenuated weight loss, reduced disease activity index, increased colon length, lowered colon macroscopic/histological scores, restored intestinal mucosal barrier and inhibited colonic inflammation. EPI (25/50 μM) had similar in vitro effects. mRNA-seq identified EPI-regulated genes in UC mice, revealing six gene clusters with analogous expression patterns. The largest cluster contained genes upregulated by DSS but downregulated by EPI, potentially involved in the MAPK pathway. Key DEGs were enriched in PI3K-Akt and MAPK pathways, verified in vivo and in vitro. Literature retrieval and molecular docking predicted glutaminyl-peptide cyclotransferase (QPCT) as EPI's potential UC therapeutic target. EPI inhibited DSS/LPS-induced QPCT upregulation in vivo and in vitro; QPCT knockdown suppressed inflammation and preserved Caco-2 monolayer barrier function, while QPCT overexpression reversed EPI's therapeutic effects. QPCT mediates PI3K-Akt/MAPK activation, and its overexpression abrogated EPI's inhibitory effects. EPI alleviates murine UC by protecting the intestinal mucosal barrier and inhibiting inflammation, likely via regulating the QPCT-PI3K-Akt/MAPK pathway. It provides a preclinical basis for developing prophylactic strategies for inflammatory bowel disease.
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PLoS One
·
2025
·Vol. 20
·期 12
·e0337214
·
IF 2.6
Ruifang Li,Yan Sun,Drolma Kelsang,Mingzhi Feng,Hanhui Cai,Jun Zhang
Background
Ulcerative colitis (UC) is an idiopathic, chronic inflammatory disease of the colon that imposes a significant global public health burden due to its recurrent and refractory nature. The therapeutic effects of butyrate on UC have been documented previously, but its specific mechanisms remain unclear.
Objective
This study aimed to investigate the effects and potential mechanisms of butyrate in dextran sulfate sodium (DSS)-induced UC.
Methods
A UC mouse model was induced utilizing 3% DSS, followed by interventions of 300 mg/kg, 600 mg/kg, or 1200 mg/kg of butyrate. The fecal condition and colonic pathology of the mice were observed, along with measurements of body weight and colon length. The expression of serum inflammatory factors, autophagy-related proteins, and the PI3K/AKT/mTOR pathway-related proteins were detected. Additionally, the impact of butyrate on the mouse gut microbial communities was evaluated using 16S rRNA sequencing technology.
Results
It was demonstrated that butyrate effectively alleviated UC symptoms, including bloody stools, weight loss, and colon shortening. Furthermore, butyrate reduced colonic tissue damage, decreased the expression of TNF-α, IL-1β, and IL-6, and significantly upregulated Beclin-1, Atg5, and the LC3II/I ratio, while reducing P62 expression. Butyrate also decreased the relative expression of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR. 16S rRNA sequencing results revealed that butyrate improved the intestinal microbial community structure by inhibiting harmful bacteria and accelerating the growth of beneficial bacteria.
Conclusion
This study suggests that butyrate may alleviate DSS-induced UC in mice by blocking the PI3K/AKT/mTOR pathway to facilitating autophagy in intestinal epithelial cells and by modulating the gut microbiota.
研究领域:
免疫学
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胃肠病学
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微生物学
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分子生物学
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营养科学
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JOURNAL OF FOOD BIOCHEMISTRY
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2026
·Vol. 2026
·期 1
·1491407
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IF 2.3
Hui Sun,Sam Al-Dalali,Fei Pan,Long Huang,Min Wei,Jinghan Wang,Rui Dai,Lingyun Wen,Miying Du,Zhigui He
This study investigated the effect of a polyphenolic ethanolic extract from Camellia nitidissima Chi (CNFC) flowers on the reduction of DSS-induced ulcerative colitis in a C57BL/6 mouse model by regulating antioxidant and anti-inflammatory mechanisms. The interaction of the fisetin molecule with essential anti-inflammatory proteins (NF-κB and NLRP3) and the antioxidant protein Keap1 was examined through molecular docking analysis. The phenolic content in CNFC was measured at 2.09 mg/g, while the flavonoid content was 2.80 mg/g. The ethanolic extract of CNFC showed IC 50 values of 0.605, 0.862, and 0.299 mg/mL against DPPH, ABTS, and OH·, respectively, indicating robust antioxidant activity. Three phenolic compounds have been identified for the first time in CNFC flowers: 6-hydroxyflavone, fisetin, and (2S,3S,4S,5R,6S)-6-[2-(3,4-dihydroxyphenyl)-5-hydroxy-4-oxochromen-7-yl]oxy-3,4,5-trihydroxyoxane-2-carboxylic acid. The model group mice experienced greater weight loss and had a colon length of 45 mm, much shorter than the intervention group’s 65 mm. The spleen inflammation index was 62.1 mg/10 g, markedly higher than the 44.2 mg/10 g in the intervention group. Additionally, the histopathology score of 7 exceeded that of the intervention group, as did the disease activity index score of 7, compared with the intervention group’s score of 1. The binding interactions of fisetin with NF-κB, Keap1, and NLRP3 proteins indicate a potential affinity for these proteins. CNFC exhibits notable antioxidant and anti-inflammatory properties, and this study offers a technical reference and theoretical foundation for advancing CNFC as a functional and therapeutic food. The present study was designed to elucidate the antioxidant and anti-inflammatory mechanisms of CNFC in DSS-induced colitis, which may serve as a reference for future studies of the multiomics profiles of CNFC’s therapeutic activity, such as gut microbiome profiling, Western blotting, and qPCR-based assessment of related gene expression, for a more detailed understanding.
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Food Bioscience
·
2026
·
IF 6.2
Chenrui Peng,Chang Lu,Xiaoting Li,Lunpu Zhang,Yao Zeng,Xiaona Wu,Ting Wu,Fang He,Xi Shen
Purpose Early-life gut microbiota establishment critically influences long-term host health. This study investigated whether maternal Bifidobacterium bifidum BD-1 supplementation during late gestation, combined with delivery mode, affects offspring responses to DSS-induced acute colitis. Methods Pregnant mice received B. bifidum BD-1 (1×10^9 CFU/day), ceftriaxone (100 mg/kg), or saline by gavage from gestational day 14 to 21. Offspring were delivered vaginally (VD) or by cesarean section (CS). Acute DSS-induced colitis was induced with 3% dextran sulfate sodium at postnatal day 42. Results VD offspring showed relatively stable microbial succession and comparatively limited variation in DSS-induced colitis-related outcomes across maternal treatment groups. In CS offspring, maternal BD-1 supplementation was associated with enrichment of beneficial genera, maintenance of α-diversity, higher fecal butyrate and propionate levels, increased expression of tight junction-related genes, and lower histopathological inflammatory scores compared with NS-CS-DSS offspring. Conclusion Maternal B. bifidum BD-1 supplementation was associated with lower indices of acute DSS-induced colitis, with more pronounced effects observed in CS offspring, supporting its potential as a prenatal probiotic candidate requiring further validation.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Xiaohu Xi,Jiankuan Li,Yingjing Wang,Yan Ni,Jiangtao Zhou,Lingya Cao,Wei Wei,Jianping Gao
Background Dextran sulfate sodium-induced ulcerative colitis is featured by excessive intestinal inflammation and disrupted mucosal immune homeostasis. Codonopsis pilosula is the sovereign herb in Shenling Baizhu Formula for ulcerative colitis therapy, and Codonopsis pilosula polysaccharides are its key active components, while their immunomodulatory effects and molecular mechanisms in Shenling Baizhu Formula against ulcerative colitis remain elusive. This study explored the critical role of Codonopsis pilosula polysaccharides and the spermidine-AMPK-mediated mitophagy-cGAS-STING inflammatory axis in regulating intestinal inflammation and ameliorating ulcerative colitis. Methods A dextran sulfate sodium-induced ulcerative colitis mouse model was established to evaluate the indispensable role of Codonopsis pilosula polysaccharides in Shenling Baizhu Formula. Ultra-high performance liquid chromatography metabolomics and 16S ribosomal RNA sequencing were performed to identify key metabolites and gut microbiota. In vitro dextran sulfate sodium-induced ulcerative colitis cellular models (human colorectal adenocarcinoma Caco-2 and human normal colonic epithelial NCM460 cells) were constructed to validate the regulatory mechanism of spermidine on AMPK-mediated mitophagy, inflammatory balance and intestinal epithelial injury. Results Codonopsis pilosula polysaccharides were essential for the anti-ulcerative colitis efficacy of Shenling Baizhu Formula: removal of Codonopsis pilosula significantly aggravated colonic pathological lesions, intestinal inflammatory responses and oxidative stress in ulcerative colitis mice, whereas Codonopsis pilosula polysaccharides supplementation reversed these abnormal phenotypes ( P < 0.05). Metabolomics and microbiomics confirmed that Codonopsis pilosula polysaccharides exerted therapeutic effects via spermidine (a key metabolite in glutamate metabolism pathway) and Muribaculaceae. Critically, in vitro dual-cell experiments verified that spermidine activated AMPK-mediated mitophagy to directly inhibit the hyperactivation of cGAS-STING inflammatory axis, thereby restoring intestinal inflammatory homeostasis and alleviating epithelial cell injury in ulcerative colitis. Conclusion Codonopsis pilosula polysaccharides extracted from the sovereign herb Codonopsis pilosula in Shenling Baizhu Formula ameliorate dextran sulfate sodium-induced ulcerative colitis, and the core mechanism depends on spermidine-triggered AMPK-mediated mitophagy to suppress the cGAS-STING inflammatory signaling axis, which plays a pivotal role in regulating intestinal immunity and repairing mucosal epithelial damage.
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JOURNAL OF MEDICINAL CHEMISTRY
·
2024
·
IF 6.8
Ruoqing Zeng,Meimiao Fang,Ancheng Shen,Xiaolei Chai,Yumiao Zhao,Mingyao Liu,Lingfeng Zhu,Weiwei Rui,Bo Feng,Liang Hong,Chunyong Ding,Zilan Song,Weiqiang Lu,Ao Zhang
Accumulating evidence has demonstrated a critical pathological role of oxysterol receptor GPR183 in various inflammatory and autoimmune diseases, including inflammatory bowel disease (IBD). However, the currently reported GPR183 antagonists are very limited and not qualified for in vivo studies due to their inferior druglike properties. Herein, we conducted a structural elaboration focusing on improving its PK and safety profile based on a reference antagonist NIBR189. Of note, compound 33, bearing an aminobenzothiazole motif, exhibited reduced hERG inhibition, improved PK properties, and robust antagonistic activity (IC50 = 0.82 nM) with high selectivity against GPR183. Moreover, compound 33 displayed strong in vitro antimigration and anti-inflammatory activity in monocytes. Oral administration of compound 33 effectively improved the pathological symptoms of DSS-induced experimental colitis. All of these findings demonstrate that compound 33 is a novel and promising GPR183 antagonist suitable for further investigation to treat IBD.
研究领域:
药理学
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免疫学
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药物化学
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高影响因子
PHYTOMEDICINE
·
2025
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IF 8.3
Yang Tang,Zheng Wang,Feng Zhou,Ling Li,Chen Sun,Linhui Li,Fei Tang,Dongqin Huang,Zewei Li,Yang Tan,Gang Pei
Background Ulcerative colitis (UC) is a clinically refractory diseases of the digestive system. Benzoylpaeoniflorin (BP) is a compound from Baishao, a Chinese herbal medicine documented with effects of anti-enteritis. However, the potential of BP in treating UC, along with its underlying mechanisms, requires further elucidation. Purpose This research was conducted to assess the effects of BP on dextran sulfate sodium (DSS)-induced UC and to elucidate its underlying mechanisms. Methods The C57BL/6 mouse model of UC was developed by administering the mice to freely drink DSS solution for 7 days. The mice were also subjected to intragastric administration of BP. Histopathology, nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, and ferroptosis indicators were determined in vivo . Besides, NCM460 cells were used to further evaluate the anti-ferroptosis effect of BP and its potential mechanisms. Ferroptosis agonists iron-dextrin (ID) and Erastin were employed to investigate whether BP exerts anti-UC effect by inhibiting ferroptosis. Similarly, Nrf2 inhibitor ML385 was conducted to ascertain the role of the Nrf2 signaling pathway in the downregulating ferroptosis effect of BP. Moreover, an ultra-performance liquid chromatography coupled with mass spectrometry was utilized to evaluate the changes in glucose metabolism within colon tissues of UC mice following BP treatment. Cellular thermal shift assay (CETSA), surface-plasmon resonance (SPR) and molecular docking were carried out to reveal the binding ability of BP and phosphogluconate dehydrogenase (PGD) protein. The PGD inhibitor, 6PGD-IN-S3 was used to evaluated whether BP inhibits anti-ferroptosis effect by upregulating the expression of PGD. Results BP exhibited significant anti-UC activity, leading to a reduction in both the disease activity index and histological damage in mice afflicted with UC. BP effectively mitigated DSS-induced ferroptosis both in vivo and in vitro . Additionally, ID and Erastin treatment diminished the therapeutic efficacy of BP against UC. A similar trend was observed in mice treated with ML385. Metabolomics analysis indicated that BP had a notable effect in restoring the pentose phosphate pathway (PPP) of colon tissues following DSS administration. The treatment of BP upregulated the activity of PGD. The inhibition of PGD weakened the anti-ferroptosis effect of BP. Subsequent analysis revealed that BP has the potential to effectively bind to PGD, thereby inhibiting PGD entries lysosomes. Conclusion The above findings provide robust evidence for the anti-UC mechanism of BP in inhibiting ferroptosis through upregulation of the Nrf2 signal. PGD, a key enzyme in the PPP, is proved as the target protein of BP to inhibit ferroptosis first time. BP has been further proved to inhibit the lysosomal degradation pathway of PGD.
研究领域:
药理学
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胃肠病学
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分子生物学
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生物化学
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中医学
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细胞生物学
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Journal of Inflammation Research
·
2025
·
IF 4.1
Yuan Zhang,Longbin Huang,Ningning Yue,Zhiliang Mai,Chen Kong,Chengmei Tian,Dao-ru Wei,Jun Yao,Lisheng Wang,Defeng Li
Background Although cytokines have been implicated in the development of ulcerative colitis (UC), the potential mediating role of metabolite levels in this association remains unclear.Methods Utilizing data from genome-wide association studies (GWAS) encompassing 91 circulating cytokines, 1400 blood metabolites, and 178,689 UC cases, we performed a two-sample Mendelian randomization (MR) analysis to investigate the effect of metabolites mediated cytokines on the development of UC. A two-step MR analysis was conducted to quantitatively evaluate the mediation effect. Additionally, dextran sodium sulfate (DSS)-induced colitis mice were used to further confirm our results.Results Mendelian randomization (MR) analysis indicated that macrophage colony-stimulating factor (M-CSF) had a causal and positive relationship with aconitate (OR: 1.10, 95% CI: 1.00–1.20, p = 0.043, IVW beta 1 = 0.095). Moreover, MR analysis revealed that high level of aconitate were associated with reduced risk of UC (OR: 0.44, 95% CI: 0.24–0.80, p = 0.008, IVW beta 2 = −0.818). In addition, MR analysis showed M-CSF had an inverse correlation with the disease onset of UC (OR: 0.31, 95% CI: 0.15–0.80, p = 0.002, IVW beta all = −1.16). Furthermore, the mediation effect of aconitate mediated M-CSF on the risk of UC was −0.0777 (95% CI: −0.154 to −0.0018, p = 0.045), accounting for 6.69% of the total effect, and indicating a modest contribution to the protective effect of M-CSF against UC. Subsequently, as an in vivo validation model, DSS-induced colitis was employed to demonstrate that M-CSF treatment significantly ameliorated weight loss, disease activity index (DAI) scores, colon shortening, and histological damage. Additionally, M-CSF treatment also significantly reduced M1 macrophage infiltration, elevated levels of aconitate as well as itaconate, and decreased the levels of pro-inflammatory cytokines in colitis. These results demonstrated that aconitate inhibited the expression of pro-inflammatory cytokines through its enzymatic conversion into the immunometabolite itaconate by aconitate decarboxylase 1 (Acod1), and downregulated the levels of M1 macrophages, thereby ameliorating colitis.Conclusion These findings suggest that M-CSF is an important anti-inflammatory cytokine in UC, which may be a promising therapeutic target in the treatment of UC.
研究领域:
免疫学
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胃肠病学
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遗传学
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代谢组学
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炎症研究
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生物医学研究
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高影响因子
International Journal of Pharmaceutics-X
·
2025
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IF 6.4
Jie-Zhou,Tian-Le Li,Bo-Wei,Yue-Feng Ruan,Ye-Qin Wang,Jiao-Yan Liu,Meng-Meng Song,Yu-Xian Shen
Midbrain astrocyte-derived neurotrophic factor (MANF) is a secreted protein induced by endoplasmic reticulum stress. Previous studies have indicated that intravenous administration of 1 mg/kg/day recombinant human MANF protein with His tag (His-MANF) for 3 days can ameliorate acute ulcerative colitis in mice. However, long-term intravenous therapy has many disadvantages. In this paper, His-MANF protein was successfully encapsulated into alginate and hyaluronic acid hybrid hydrogel microcapsules in one step using the gas shear method and then coated by Eudragit S100 to construct an oral colon-targeted delivery system (MSH@E). The MSH@E microcapsules exhibited controlled and sustained release behavior and colon-targeting properties. Both fluorescent imaging and immunohistochemistry staining results showed that His-MANF protein could accumulate in the colitis colon for a longer residence time after oral delivery. In vivo studies demonstrated that oral administration of MSH@E microcapsules could alleviate DSS-induced colitis in mice without systemic toxicity. Importantly, even if the oral His-MANF dose was half of the intravenous His-MANF dose, oral delivery was still much more effective than intravenous injection, suggesting the development of the oral colon-targeted delivery system (MSH@E) has great significance and makes a breakthrough from intravenous to oral administration for His-MANF treatment of ulcerative colitis (UC).
研究领域:
药剂学
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胃肠病学
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药物递送系统
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生物医学工程
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高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2024
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IF 4.8
Nannan Peng,Jingmin Wang,Haimei Zhu,Ziyue Liu,Jiayi Ren,Wenjing Li,Yongzhong Wang
Inflammatory bowel disease (IBD) is a recurrent chronic colitis disease with increasing incidence and prevalence year by year. The single efficacy and significant side effects of traditional IBD treatment drugs have promoted the flourishing development of new drugs. Inspired by many health benefits of carbon dots (CDs) based nanomedicine in biomedical applications, a metal-free carbon dots (CP-CDs) was synthesized from citric acid and polyethylene polyamine to treat colitis. Oxidative stress tests at the cellular and nematode levels demonstrated CP-CDs have good antioxidant effects, while the toxicity of CP-CDs to cells and nematodes is low. CP-CDs were further applied to dextran sodium sulfate (DSS)-induced colitis in mice models, and it was found that CP-CDs can reduce the disease activity index (DAI) score of colon tissue and restore the intestinal barrier. Further, the anti-colitis mechanisms of CP-CDs were explored, one of which is to regulate intestinal oxidative stress in inflammatory mice, further reducing the expression of inflammatory cytokines, and thus alleviating colitis. Notably, 16S rRNA sequence analysis showed that the abundance of beneficial bacteria ( Ligilactobacillus and Enterorhabdus ) in the intestinal tract increased, while that of harmful bacteria ( unclassified_Clostridia_UCG_014 ) decreased after CP-CDs treatment, indicating that CP-CDs rebalancing the gut microbiota destroyed by DSS is another important mechanism. In short, these non-toxic carbon dots not only have the potential for multi-factor combined relief of colitis but also offer an alternative therapy medicine for patients suffering from IBD.
研究领域:
药理学
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胃肠病学
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纳米医学
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微生物学
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免疫学
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
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IF 7.7
Liang Guo,Ge-Ge Zheng,Rong-Yi Li,Cheng-yu Fu,Jie Chen,Yue-Cheng Meng,Yang Pan,Po Hu
Ulcerative colitis (UC) stands as a chronic inflammatory intestinal disease. This study aimed to explore a sustained-release strategy to alleviate DSS-induced colitis in mice using polyelectrolyte complexes (PECs) encapsulating an alkaloid, isoliensinine (ISO). The drug delivery platform, termed “Saloplastics (SAL)”, was prepared by fabrication of PECs through the solid-liquid phase separation of sodium caseinate (SC) and ε-polylysine (EPL), followed by centrifugation to yield compact structures. Coarse-grained molecular dynamics simulations demonstrated that SAL had a nanorod-like structure formation between EPL and SC, which implied that the self-assembly of SAL is driven by hydrophobic aggregation and strong electrostatic attractions. A comprehensive evaluation of SAL was conducted, including characterizations of its physicochemical and biological properties. The results showed SAL had thermal plasticization properties and excellent swelling capacity as well as susceptibility to hydrolysis by pH and proteinase in simulated gastric fluid. Moreover, SAL displayed a porous morphology with high surface area for immobilizing organic molecules. ISO@SAL, formulated by ISO encapsulated in SAL, not only demonstrated high potency in alleviating DSS-induced colitis in mice, but also increased the dosing intervals from one day to three days. In conclusion, SAL is a biocompatible sustained-release oral drug delivery platform for gastrointestinal applications.
研究领域:
药剂学
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药理学
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生物技术
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胃肠病学
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