Diabetic hepatic injury is a common complication of diabetes, yet it is often neglected due to its subtle early symptoms. This study explored the effect and mechanism of Anaphalis virgata extract (AVE) in treating diabetic hepatic injury. Serum-exposed components of AVE were identified by LC-MS and used for network pharmacology to predict therapeutic targets and pathways. AVE was evaluated in diabetic rats treated intragastrically at 50, 100, and 200 mg/kg for 10 weeks. Hepatic biochemical parameters were measured, and mechanisms were verified by molecular dynamics (MD) simulation, ELISA, and Western blot. Thirty-one serum-exposed compounds (8 prototypes and 23 metabolites) were identified, primarily flavonoids, phenolic acids, terpenoids, and phenylpropanoids. Network pharmacology revealed pathways including lipid and atherosclerosis, IL-17, and AGE-RAGE signaling. Apigenin, kaempferol, and caffeic acid were identified as core compounds, and IL-6, TNF, and IL-1β as core targets. In vivo, AVE significantly decreased hepatic IL-6, TNF, IL-1β, TC, TG, FFA, AST, and ALT levels in diabetic rats. Western blot showed that AVE up-regulated AKT and AMPK while down-regulating NF-κB and GSK-3β pathways. AVE exerts a therapeutic effect on diabetic hepatic injury through anti-inflammatory mechanisms, providing a foundation for its further development and clinical application.

Diabetic nephropathy (DN) is a severe diabetic complication with substantial clinical burden. The complex pathogenesis of DN has hindered the development of targeted therapies, creating an urgent need to develop novel strategies that directly address its underlying inflammatory and fibrotic mechanisms. Coreopsis tinctoria (CE) is an edible plant rich in polyphenols, but its mechanism against DN remains understood. An integrated framework combining network pharmacology and machine learning was developed to prioritize active polyphenols and their targets. A multi-layer perceptron classifier, trained on 3.16 million compound–target pairs from Binding DB, predicted interactions between 36 CE polyphenols and 12,030 DN-associated genes. The top 100 targets were subjected to KEGG enrichment analysis, and the identified pathways were validated in a high-fat diet/STZ-induced DN rat model. The MLP model achieved superior performance (AUC-ROC = 0.9219, AP = 0.9592). Five lead polyphenols (flavonoids/chalcones) showed high predicted activity. KEGG analysis revealed enrichment in PI3K-Akt, calcium signaling, metabolic pathways, and cellular senescence. In vivo, CE treatment (150–600 mg/kg/day) dose-dependently improved glucose/lipid metabolism and renal function, and ameliorated histopathological damage, including glomerular hypertrophy, fibrosis, and mesangial expansion. Mechanistically, CE suppressed NFκB/TGFβ/Smad signaling, restored PPARγ and Nrf2/HO-1/FoxO1 antioxidant defenses, and inhibited apoptosis via Bcl-2/Bax regulation. CE exerts multi-target renoprotective effects through coordinated modulation of metabolic, inflammatory, fibrotic, and antioxidant pathways, supporting its potential as a functional food ingredient for DN management.

ETHNOPHARMACOLOGICAL RELEVANCE:Anterior uveitis (AU) is the prevalent form of uveitis among ocular disease. Shabyar (SBY), as a traditional central asian ethnic medicine, has been used in the treatment of ocular diseases. However, its potential mechanism of action in treating AU remains unclear. AIM OF THE STUDY:This study aimed to investigate the therapeutic effect and related mechanisms of SBY on endotoxin-induced uveitis (EIU) in male rats. MATERIALS AND METHODS:Network pharmacology (NP) was applied to identify the potential pharmacological target network of SBY in treating EIU. Commercial assay kits were used to measure the levels of inflammatory markers and vascular regulators. The leakage of Evans blue (EB) in retina was quantitatively assessed. Immunohistochemistry was performed to evaluate the relative expression of JAK2, p-JAK2, STAT3, and p-STAT3 in retinal tissues. Western blotting was conducted in lipopolysaccharide (LPS)-stimulated RAW264.7 cells to investigate the effects of SBY on the JAK2/STAT3 pathway. RESULTS:SBY alleviated inflammation in EIU male rats by reducing inflammatory cell infiltration and cytokine release, an effect potentially related to suppression of JAK2/STAT3 pathway activation. Correspondingly, in LPS-induced RAW264.7 cells, SBY's anti-inflammatory action involved regulation of the JAK2/STAT3 pathway. Moreover, SBY inhibited the level of VEGF, upregulated PEDF expression, and thereby alleviated blood-retinal barrier (BRB) leakage and retinal edema in EIU male rats. CONCLUSION:The protective effects of SBY on EIU in male rats may be mediated through the involvement of the JAK2/STAT3 and VEGF pathways. However, it should be noted that the absence of a direct comparison with a standard clinical corticosteroid (e.g., dexamethasone) in the in vivo study limits to some extent the immediate clinical potency benchmarking of SBY.

In order to isolate and characterize enantiomeric compounds from the roots of Prangos pabularia the dichloromethane extract was extensively fractionated by column chromatography, flash, semi-preparative high performance liquid chromatography (HPLC), and chiral HPLC. Six pairs of enantiomers were isolated from dichloromethane extracts using preparative chiral HPLC. The absolute configurations of the isolated isomers were identified using circular dichroism (CD). The anti-vitiligo activities of the corresponding (S)- and (R)-enantiomers were assessed by determining their tyrosinase activation rates. (S)-Pangelin 9 (PPE19-1) showed higher activity with 125.42% than (R)-pangelin 10 (PPE19-2) with 120.6%, while the positive control (8-methoxypsoralen) resulted in 122.3%. The percentage of activation rate of (S)-oxypeucidanin hydrate 1 (PPE4-1) was 119.74%, while it was 110.01% for (R) oxypeucidanin hydrate 2 (PPE4-2). We conclude that the (S, R) enantiomers of pangelin and oxypeucidanin hydrate (S, R) may be useful as pigmentation-promoting agents for the treatment of vitiligo.

Background:Metabolic dysfunction-associated steatohepatitis (MASH) is the most prevalent chronic liver disease worldwide; however, few effective therapeutic options are available for MASH. Artemisia scoparia is a medicinal plant that has been widely utilized in traditional medicine to treat liver-related ailments. Nonetheless, the effects and underlying mechanisms of A. scoparia in the context of MASH remain poorly understood. Aim of the study:The objective of this research was to assess the protective effects and further mechanisms of A. scoparia extract (AS) on a MASH mice model. Methods:The protective effects of AS were evaluated both in vivo and in vitro, with the therapeutic efficacy of AS being characterized through the detection of biochemical markers, histological analysis, and Oil red O staining. To elucidate the underlying mechanisms and pharmacodynamic basis of AS, a comprehensive set of techniques were applied, including transcriptomics, metabolomics, Western blotting, and immunofluorescence staining. Results:AS reduced the blood lipid indices and inflammatory levels in the MASH mouse model and decreased lipid droplet accumulation in FFA-induced HepG2 cells. Transcriptomic and metabolomic analyses indicated that AS regulates 30 dysregulated genes (e.g., Gm15622, Pdia6, and Derl3) and controls 60 metabolic metabolites (e.g., heptadecanoic acid, 5b-cyprinol sulfate, and taurodeoxycholic acid) to ultimately affect core pathways involved in lipid metabolism and inflammation. Furthermore, AS was proven to exert a hepatoprotective effect by inhibiting inflammation and ferroptosis, along with weakening the advanced glycation end product-receptor for advanced glycation end products (AGE-RAGE) pathway and the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway in vivo and in vitro. Conclusion:This study first elucidates the mechanism through which AS ameliorates MASH through integrated multi-omics analysis, providing experimental evidence for further development of natural therapeutic agents.

Rosa rugosa Thunb., Punica granatum L., and Cichorium glandulolsum Boiss. et Huet. are traditional herbal medicine, which can treat diabetes and diabetes complications, a formulation named RPC is composed of these three plants. The aim of this study was to investigate the chemical constituents and potential pharmacological mechanisms of RPC in treating diabetes. RPC significantly inhibited the activities of α-glycosidase and PTP1B, and has good activity of free radical scavenging. The main chemical constituents of PRC were analyzed by HPLC-QTOF-MS, a total of 45 constituents were identified. The key targets and main signaling pathways were predicted by network pharmacology. Experimental validation revealed that RPC enhanced glucose consumption and uptake while mitigating oxidative stress in L6 cells. Notably, signaling pathways such as PI3K/AKT/FoxO1, AMPK/Nrf2/HO-1, and endoplasmic reticulum stress pathways, as predicted by network pharmacology, were also markedly induced by RPC. In the animal experiment, four weeks of RPC treatment resulted in significant reductions in blood glucose and lipid profiles, along with improvements in glucose tolerance, insulin tolerance, antioxidant enzymes, and glycogen synthesis in db/db mice. The observed hypoglycemic effect of RPC may be attributable to the combined effects of signaling pathways regulating glucose metabolism, energy sensing and inhibition of oxidative stress.

IntroductionAlcoholic liver disease (ALD) is a serious global health burden with limited effective therapies. 4,5-Dicaffeoylquinic acid (DCA-C), a monomer from Artemisia scoparia, exhibits multiple bioactivities, but its protective effects and exact mechanisms against ALD remain unclear.MethodsEthanol-induced ALD mouse models were treated with DCA-C at 10, 30, and 100 mg/kg. Liver injury, lipid accumulation, and inflammation were evaluated. Transcriptomic sequencing and molecular docking were used to identify key targets. PLA2G4B overexpression models in vitro and in vivo were constructed to validate the mechanism.ResultsDCA-C dose-dependently alleviated alcoholic liver injury, with the 100 mg/kg dose being most effective, as shown by reduced serum ALT/AST, decreased hepatic triglycerides, and suppressed pro-inflammatory cytokines. PLA2G4B was identified as a core target of DCA-C. DCA-C directly bound PLA2G4B, downregulated its expression, and reduced arachidonic acid (AA) release, thereby inhibiting MAPK signaling (ERK, p38, JNK phosphorylation). PLA2G4B overexpression abolished the protective effects of DCA-C in vitro and in vivo.DiscussionDCA-C protects against ALD via targeting PLA2G4B and inhibiting the AA-MAPK pathway. DCA-C is a promising candidate for ALD treatment and warrants further development.

Ela tablets (ALP) is a traditional Uyghur medicinal formulation comprising 9 herbs. Clinical applications have demonstrated its potential in treating diabetic nephropathy (DN). However, its specific medicinal effects and pharmacodynamic components have not been elucidated. This research aims to investigate the efficacy of ALP in treating DN and to explore the quality markers (Q-markers) for its exertion of efficacy. Using the UHPLC-Q-Orbitrap HRMS technique, a total of 60 compounds were identified within ALP. Animal experiments were conducted to investigate the effect of ALP intervention at doses of 80, 160, and 320 mg/kg in Sprague-Dawley rats. Then, fingerprints of ten batches of ALP extracts were established using UPLC-DAD. Spectrum-effect relationship analysis of these fingerprints and aldose reductase (AR) activity was conducted by chemometric analysis methods. The results were further validated by molecular docking and cellular experiments. The animal experiments indicated that ALP had a therapeutic effect on DN. Specifically, ALP reduced biochemical indexes such as serum creatinine (SCr), 24-hour urinary total protein (24 h UTP), uric acid (UA), blood urea nitrogen (BUN), triglycerides (TG), and total cholesterol (TC). ALP stabilized body weight and fasting blood glucose, enhanced the antioxidant capacity of kidneys, and improved renal pathology. Comprehensive analysis indicated that crocin-I and gallic acid may be used as Q-markers for ALP. In summary, ALP has been identified as a treatment for DN, and gallic acid and crocin-I can be used as its Q-markers.

Chemical investigations of the n-butanol extract of the roots of Prangos pabularia were carried out using column chromatography, flash, semi-preparative HPLC, and chiral HPLC. Five unidentified compounds, including two prenylated coumarin glucosides, two prenylated furanocoumarin glucosides, and a benzofuran glucoside, together with twelve known compounds, were isolated from the n-butanol fraction of P. pabularia extract. The structures of these compounds were identified by HRMS, NMR, UV, ECD in combination with quantum chemical calculations, and comparison with the literature. The new compounds were named as yuganins C-G (1-5). Yuganin C (1) and yuganin D (2) are C-prenylated coumarin glucosides, yuganin E (3) is an 8-O-prenylated furanocoumarin glucoside, yuganin F (4) is a furanocoumarin 5-O-glucoside, and yuganin G (5) is a benzofuran glucoside. The isolated compounds were evaluated for their anti-vitiligo activity. All the individual isolated compounds showed anti-vitiligo effects. Compounds 10, 12, and 13 showed the highest melanin rate activation.

Diabetic retinopathy (DR) is a specific microvascular problem of diabetes, which is mainly caused by hyperglycemia and may lead to rapid vision loss. Dietary polyphenols have been reported to decrease the risk of DR. Apocynum venetum L. leaves are rich in polyphenolic compounds and are popular worldwide for their health benefits as a national tea drink. Building on previous findings of antioxidant activity and aldose reductase inhibition of A. venetum, this study investigated the chemical composition of polyphenol-rich extract of A. venetum leaves (AVL) and its protective mechanism on ARPE-19 cells in hyperglycemia. Ninety-three compounds were identified from AVL by LC-MS/MS, including sixty-eight flavonoids, twenty-one organic acids, and four coumarins. AVL regulated the polyol pathway by decreasing the expression of aldose reductase and the content of sorbitol, enhancing the Na+K+-ATPase activity, and weakening intracellular oxidative stress effectively; it also could regulate the expression of autophagy-related proteins via the AMPK/mTOR/ULK1 signaling pathway to maintain intracellular homeostasis. AVL could restore the polyol pathway, inhibit oxidative stress, and maintain intracellular autophagy to protect cellular morphology and improve DR. The study reveals the phytochemical composition and protective mechanisms of AVL against DR, which could be developed as a functional food and/or candidate pharmaceutical, aiming for retina protection in diabetic retinopathy.

Six undescribed sesquiterpene lactones (1-6) and fifteen known compounds (7-21) were isolated from Seriphidium transiliense. The chemical structures were determined by extensive NMR spectroscopic data, HRESIMS, ECD and X-ray diffraction. Among the known compounds, twelve known compounds were isolated for the first time from this plant, including taurine (9), 11-epitaurin (10), α-santonin (11), artesin (13), 11-epiartesin (14), 1α-hydroxy-3β-acetoxyeudesm-4-en-6β, 7α, 11βH-12, 6-olide (15), 1α-hydroxy-3β-acetoxyeudesm-4-en-6β, 7α, 11αH-12, 6-olide (16), artegallin (17), 8α-hydroxytaurin (18), 8α-acetoxytaurine (19), methyl-4α-hydroxy-11(13)-eudesmen-12-oatesaniculamoid D (20), and saniculamoid D (21). The absolute configuration of 2 was determined by X-ray. The X-ray crystal structures of 15 and 16 were reported for the first time. At a concentration of 20 μM, all compounds (1-21) showed significant inhibition of NO production in LPS- stimulated BV2 cells. Among them, compounds 3 and 4 inhibited NO release with IC50 values of 19.30 and 22.05 μM, respectively. Based on the present results, these compounds may be potential anti-inflammatory agents.

Four undescribed sesquiterpene compounds (1-4) 1 - 4 ) and six known compounds (5-10) 5 - 10 ) were isolated from A. mongolica. . Furthermore, compound 5 was a new natural product previously synthesized. The LPS-stimulated BV2 cells were used as a model to evaluate the anti-inflammatory activity of the isolated compounds, among them, compounds 2 , 3 and 4 showed significant inhibition of NO levels with IC50 50 values of 27.48, 27.39 and 24.96 mu M, respectively.

Nine previously undescribed brefeldin A (BFA) derivatives (1-9), together with one known compound 4-epibrefeldin A (10), were isolated from an endophytic fungus Penicillium brefeldianum F4a. The chemical structures were elucidated using NMR and HRESIMS. ECD analysis and Mosher's method were used to confirm the absolute configurations of 1-9. The inhibitory activity of all isolated BFA derivatives (1-10) on acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) was evaluated in vitro. The bioassay results suggested that neobrefeldin (1) and brefeldin H (2) exhibited higher potent and selective AChE inhibitory activity (IC50 = 0.12 and 0.28 mu M) than the therapeutic drug galantamine for Alzheimer's disease (AD) (IC50 = 0.66 mu M), whereas only neobrefeldin (1) displayed weak inhibitory activity against BuChE (IC50 = 175.04 mu M). Moreover, a molecular docking analyses was performed and showed compounds 1 and 2 were dual binding site AChE inhibitors. It is worth noting that neobrefeldin (1) showed a better binding affinity with the peripheral anionic site through the hydrogen bonding interaction with Tyr124 than brefeldin H (2), resulting in better AChE inhibitory activity. These findings not only provide a promising AChE inhibitor neobrefeldin (1) for developing agents against early AD, but also provide a valuable perspective for better understanding its AChE inhibition activity.

Ethnopharmacological relevance: Artemisia mongolica is well known for its use in folk medicine, it is commonly used to alleviate a variety of diseases associated with inflammation, such as laryngitis, tonsillitis, headaches and hepatitis in northwest China. However, its anti-inflammatory mechanism is still unknown. Aim of the study: The most potential anti-inflammatory part (AMPA) was identified by screening individual parts of A. Mongolica. After the network pharmacological analysis, the anti-inflammation effects and molecular mechanisms of AMPA were evaluated in RAW264.7 cells induced by LPS. Materials and methods: AMPA was chosen as the most anti-inflammatory of the A. Mongolica, as measured by the effect of each part of the A. Mongolica on NO and COX-2. The chemical composition of AMPA was identified using HPLC-Q-TOF-MS/MS, and targets of bioactive chemicals and targets related to inflammation were found using open-source databases. The "Compound-targets" network and PPI network were established by combining compounds and overlapped targets, and targets in the PPI networks were analyzed by GO and KEGG enrichment. The RAW26.7 cells induced by LPS were used as a model of inflammation examination. MTT assay was performed to assess the cytotoxicity of AMPA on LPS-induced RAW264.7 cells. The level of NO was measured by the Griess method while the inflammatory factors were detected by ELISA. The protein expression levels of iNOS, COX-2, MAPK, NF-kappa B signaling pathway and AMPK/Nrf2-related proteins were determined by Western blot. The results of nuclear translocation of p65 and Nrf2 were analyzed by immunofluorescence assay. Results: A total of 18 compounds with potential bioactivity were identified, and after intersecting 640 compoundpredicted targets and 1608 inflammation targets, the compounds and intersected targets were utilized to structure "compound-target" and PPI networks. Among AMPA, AM6, AM7, AM11, AM8 and AM1 compounds were essential in the "compound-targets" network, meanwhile, TNF, RELA, MAPK1, NOS2, PRKAG, and PTGS2 targets play important roles in the PPI network. The top 10 terms and pathways were obtained based on GO and KEGG. The cell experiments show that 50 mu g/mL was the maximum concentration of AMPA without cytotoxicity in the LPS-induced RAW264.7 cell model. When compared with the LPS group, AMPA treatment not only effectively suppressed the generation of NO, TNF-alpha, IL-6, PGE2, IL-1 beta and MCP-1 in LPS-induced RAW264.7 cells, but also down-regulated the expression of COX-2, iNOS and the protein levels p-ERK, p-p38, p-I kappa B-alpha and p-p65, inhibited the nuclear translocation of p65. Furthermore, the expression levels of p-LKB1, p-AMPK, Nrf2 and HO-1 proteins were up-regulated and Nrf2 nuclear translocation was promoted. Conclusion: AMPA should be considered an anti-inflammatory agent for the results of network pharmacology and in vitro, which could inhibit the MAPK pathway and NF-kappa B pathway and activate the AMPK/Nrf2 pathway in LPS-stimulated RAW264.7 cells.

Terminalia chebula Retz. is commonly used in the treatment of diabetes, but its specific ingredients and hypoglycaemic mechanisms remain unclear. In this study, spectrum-effect relationships between common peaks of fingerprint and DPPH, ABTS, PTP1B, α-glucosidase, were used to screen six compounds as the potential hypoglycemic ingredients. Molecular docking studies were conducted on chebulagic acid, chebulinic acid and punicalagin, which were identified by reference standard, revealing the potent in teractions between these bioactive substances and the PTP1B, α-glucosidase protein. Additionally, the cellular level results showed that punicalagin displayed stronger inhibition of PTP1B and α-glucosidase, with IC50 values of 0.0236 and 0.335 μg/mL, respectively, while improving glucose consumption and intracellular glycogen content of insult-resistant L6 muscle cell, and the hypoglycemic effect was achieved by activating the PI3K/AKT signaling pathway. This study demonstrated that T. chebula has the potential to become a hypoglycemic functional food, and offers a strategy for characterization hypoglycemic ingredients.

In the current study, the lipophilic solvent (n-hexane) extraction, steam distillation (SD) and supercritical CO2 fluid extraction (SC-CO2) methods were used to extract the volatile components of Mentha asiatica Boriss. Comparisons were made between the extraction yield, chemical component and biological activity. Gas chromatography quadrupole-time-of-flight mass spectrometry (GC-QTOF-MS) and semi-quantitative analysis of chemical contents by flame ionization detector (GC-FID) were used to study the chemical ingredients in Mentha asiatica Boriss. aromatic extract. The oil extract obtained from lipophilic solvent (n-hexane) extraction (1.27 +/- 0.03%, w/W) showed the highest yield, followed by supercritical CO2 fluid extraction (1.15 +/- 0.04%, w/W), the extraction rate of SD was (0.37 +/- 0.01%?w/W). The oil extract of Mentha asiatica Boriss. contained a total of 70 components that were identified. In the following, the primary volatile compounds of the essential oil produced using the three extraction techniques: alpha-thujene, camphene, sabinene, beta-pinene, beta-cymene, limonene, beta-terpinene, camphol, alpha-terpinene, carvenone, carvone, piperitone oxide, thymol, myrtenyl acetate, dihydrojasmone, caryophyllene, germacrene D and caryophyllene oxide. Findings from this study indicate that the three methods of essential oil extraction produced oils with varying antioxidant capacities against DPPH and ABTS free radicals. Against Staphylococcus aureus, Candida albicans, Bacillus subtilis and Escherichia coli, all of the essential oils simultaneously showed clear inhibitory actions. Response surface methodology (RSM) and the Box-Benhnken design with three factors and three levels were both utilized to optimize the distillation process of essential oils. The appropriate extraction parameters were a 3 h extraction period, a solid-liquid ratio of 1:10 and a 3 h soaking time. The highest yield of essential oil was 0.38%. The impact of extraction parameters on essential oil yield was examined using the SD method. The findings indicated that the main factors affecting the yield of volatile oil extracted by SD were soaking time > ratio of solid to liquid > extraction time.

Neuroinflammation is a causative factor in neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis. Previous studies have shown that Artemisia mongolica has anti-inflammatory properties. Aschantin (AM3) has been shown to have anti-inflammatory effects. However, the mechanism of AM3 and its epimer epi-aschantin (AM2) remains controversial. Therefore, the present study explored the mechanism of neuroinflammation by AM2 and AM3 and attempted to reveal the relationship between the structure of AM2 and AM3 and anti-neuroinflammatory activity. We isolated for the first time 12 lignans from A. mongolica that inhibited NO content at 10 mu M in LPS-stimulated BV2 cells. Among them, epi-aschantin (AM2) and Aschantin (AM3) showed significant inhibition in NO screening. With further studies, we found that both AM2 and AM3 effectively inhibited the overproduction of NO, PGE2, IL-6, TNF-alpha and MCP-1, as well as the overexpression of COX-2 and iNOS. Mechanistic studies have shown AM2 and AM3 significantly inhibited the phosphorylation of ERK, JNK and P-38 in the MAPK signaling pathway and p-I kappa B alpha,p-p65 and blocked p65 entry into the nucleus. The results suggested that the pair of epimers (AM2 and AM3) can be used as potential therapeutic agents in the treatment of various brain disorders and that structural differences do not differ in anti-neuroinflammatory effects.

Seven compounds were isolated from Seriphidium transiliense, of which 1–5 and 7 were obtained for the first time. Compound 1 was a new natural compound that was previously synthesized. Compounds 4, 5, and 7 in LPS-stimulated BV2 cells inhibited the NO content with IC50 42.24, 44.03, and 35.67 μM, respectively.

Prunus cerasifera Ehrhart fruit polysaccharide (PCP) was obtained after determining the optimal extraction conditions for complex enzyme-assisted hot buffer extraction based on single-factor experiments and response surface methodology, followed by characterization of its physicochemical, processing, rheological, and biological properties. PCP was a thermally stable carbohydrate with acidic functional groups and a molecular weight of 1398.69 kDa, exhibiting smooth, dense flake and honeycomb network microstructures. PCP had favorable hygroscopicity, moisturizing properties, water and oil-holding capacity, proemulsification capability, and in vitro antioxidant activity. The apparent viscosity of PCP in an aqueous system was dependent on concentration and temperature and was altered by the variety and amount of metal ions added; its aqueous solutions exhibited strong viscosity and hydrogel-forming tendencies at suitable concentrations, along with excellent hydrogel properties after gelation. Furthermore, PCP favored the growth of beneficial gut microbiota and associated microbes responsible for producing essential short-chain fatty acids. Overall, PCP displayed high potential as a multifunctional additive for applications in the food, pharmaceutical, and cosmetic industries.