Biogenic selenium nanoparticles alleviate intestinal barrier injury in mice through TBC1D15/Fis1/Rab7 pathway.

Intestinal diseases often stem from a compromised intestinal barrier. This barrier relies on a functional epithelium and proper turnover of intestinal cells, supported by mitochondrial health. Mitochondria and lysosomes play key roles in cellular balance. Our previous researches indicate that biogenic selenium nanoparticles (SeNPs) can alleviate intestinal epithelial barrier damage by enhancing mitochondria-lysosome crosstalk, though the detailed mechanism is unclear. This study aimed to investigate the role of mitochondria-lysosome crosstalk in the protective effect of SeNPs on intestinal barrier function in mice exposed to lipopolysaccharide (LPS). The results showed that LPS exposure increased intestinal permeability in mice, leding to structural and functional damage to mitochondrial and lysosomal. Oral administration of SeNPs significantly upregulated the expression levels of TBC1D15 and Fis1, downregulated the expression levels of Rab7, Caspase-3, Cathepsin B, and MCOLN2, effectively alleviated LPS-induced mitochondrial and lysosomal dysfunction and maintained the intestinal barrier integrity in mice. Furthermore, SeNPs notably inhibited mitophagy caused by adenovirus-associated virus (AAV)-mediated RNA interference the expression of TBC1D15 in the intestine of mice, maintained mitochondrial and lysosomal homeostasis, and effectively alleviated intestinal barrier damage. These results suggested that SeNPs can regulate mitochondria-lysosome crosstalk and inhibit its damage by regulating the TBC1D15/Fis1/Rab7- signaling pathway. thereby alleviating intestinal barrier damage. It lays a theoretical foundation for elucidating the mechanism of mitochondria-lysosome crosstalk in regulating intestinal barrier damage and repair, and provides new ideas and new ways to establish safe and efficient nutritional regulation strategies to prevent and treat intestinal diseases caused by inflammation.

Targeting mitochondria with antioxidant nutrients for the prevention and treatment of postweaning diarrhea in piglets.

Post-weaning diarrhea (PWD) in piglets poses a significant challenge and presents a grave threat to the global swine industry, resulting in considerable financial losses and compromising the welfare of animals. PWD is commonly associated with gut homeostatic imbalance, including oxidative stress, excessive inflammation, and microbiota dysbiosis. Antibiotic use has historically been a common initiative to combat PWD, but concerns about the development of antibiotic resistance have led to increased interest in alternative strategies. Mitochondria are key players in maintaining cellular homeostasis, and their dysfunction is intricately linked to the onset and progression of PWD. Accumulating evidence suggests that targeting mitochondrial function using antioxidant nutrients, such as vitamins, minerals and polyphenolic compounds, may represent a promising approach for preventing and treating PWD. Moreover, nutrients based on antioxidant strategies have been shown to improve mitochondrial function, restore intestinal redox balance, and reduce oxidative damage, which is a key driver of PWD. The present review begins with an overview of the potential interplay between mitochondria and gut homeostasis in the pathogenesis of PWD in piglets. Subsequently, alternative strategies to prevent and treat PWD using antioxidant nutrients to target mitochondria are described and discussed. Ultimately, we delve into potential limitations and suggest future research directions in this field for further advancement. Overall, targeting mitochondria using antioxidant nutrients may be a promising approach to combat PWD and provides a potential nutrition intervention strategy for regulating gut homeostasis of weaned piglets.

Replacing dietary sodium selenite with biogenic selenium nanoparticles improves the growth performance and gut health of early-weaned piglets.

Selenium nanoparticles (SeNPs) are proposed as a safer and more effective selenium delivery system than sodium selenite (Na2SeO3). Here, we investigated the effects of replacing dietary Na2SeO3 with SeNPs synthesized by Lactobacillus casei ATCC 393 on the growth performance and gut health of early-weaned piglets. Seventy-two piglets (Duroc × Landrace × Large Yorkshire) weaned at 21 d of age were divided into the control group (basal diet containing 0.3 mg Se/kg from Na2SeO3) and SeNPs group (basal diet containing 0.3 mg Se/kg from SeNPs) during a 14-d feeding period. The results revealed that SeNPs supplementation increased the average daily gain (P = 0.022) and average daily feed intake (P = 0.033), reduced (P = 0.056) the diarrhea incidence, and improved (P = 0.013) the feed conversion ratio compared with Na2SeO3. Additionally, SeNPs increased jejunal microvilli height (P = 0.006) and alleviated the intestinal barrier dysfunction by upregulating (P < 0.05) the expression levels of mucin 2 and tight junction proteins, increasing (P < 0.05) Se availability, and maintaining mitochondrial structure and function, thereby improving antioxidant capacity and immunity. Furthermore, metabolomics showed that SeNPs can regulate lipid metabolism and participate in the synthesis, secretion and action of parathyroid hormone, proximal tubule bicarbonate reclamation and tricarboxylic acid cycle. Moreover, SeNPs increased (P < 0.05) the abundance of Holdemanella and the levels of acetate and propionate. Correlation analysis suggested that Holdemanella was closely associated with the regulatory effects of SeNPs on early-weaned piglets through participating in lipid metabolism. Overall, replacing dietary Na2SeO3 with biogenic SeNPs could be a potential nutritional intervention strategy to prevent early-weaning syndrome in piglets.

Selenium nanoparticles alleviate deoxynivalenol-induced intestinal epithelial barrier dysfunction by regulating endoplasmic reticulum stress in IPEC-J2 cells.

The intestinal epithelial barrier plays a crucial role in maintaining human and animal health. Deoxynivalenol (DON) is a mycotoxin that contaminates cereal-based foods worldwide, which is a serious threat to human and animal health. This study was aimed to investigate the protective effect of selenium nanoparticles (SeNPs) synthesized by Lactobacillus casei ATCC 393 against DON-induced intestinal epithelial barrier dysfunction and its relationship with PERK-mediated signaling pathway. IPEC-J2 cells were randomly assigned to four groups: Con (vehicle), DON (0.6 µg DON/mL, 48 h), SeNPs+DON (8 µg Se/mL, 24 h; 0.6 µg DON/mL, 48 h) and SeNPs (8 µg Se/mL, 24 h). Compared with Con group, the transepithelial electrical resistance (TEER) and the tight junction proteins expression of IPEC-J2 cells exposed to DON was increased and decreased, respectively. In addition, DON exposure led to increased ROS content, decreased antioxidant capacity, structural damage of endoplasmic reticulum (ER), and activation of endoplasmic reticulum stress (ERS)-related protein kinase R-like endoplasmic reticulum kinase (PERK) pathway in IPEC-J2. Compared with SeNPs+DON group, SeNPs alleviated oxidative stress, ER structure damage and PERK pathway activation and the increase of intestinal epithelial permeability of IPEC-J2 cells exposed to DON. PERK agonist (CCT020312) and inhibitor (GSK2656157) treatments were performed to identify the role of PERK signaling pathway in the regulatory effects of SeNPs on DON-induced intestinal epithelial barrier dysfunction. Compared with SeNPs+DON group, PERK agonist increased the expression levels of p-PERK. PERK inhibitor exerted a similar inhibitory effect to SeNPs on the p-PERK expression. In conclusion, SeNPs effectively alleviate DON-induced intestinal epithelial barrier dysfunction in IPEC-J2 cells, which are closely associated with ERS-related PERK signaling pathway. This will provide a potential solution for prevention and control of DON in the aquaculture industry.

Lactobacillus casei ATCC 393 combined with vasoactive intestinal peptide alleviates dextran sodium sulfate-induced ulcerative colitis in C57BL/6 mice via NF-κB and Nrf2 signaling pathways.

Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) which is related to an immunological imbalance of the intestinal mucosa. Many clinical evidences indicate probiotics supplementation appears to be effective and safe in patients with UC. Vasoactive intestinal peptide (VIP) is an endogenous neuropeptide with multiple physiological and pathological effects. In this study, we investigated the protective effect of the combination of Lactobacillus casei ATCC 393 (L. casei ATCC 393) with VIP on dextran sodium sulfate (DSS)-induced UC in mice and the potential mechanism. The results showed that, compared with the control group, DSS treatment significantly shortened the colon length, caused inflammation and oxidative stress, and further resulted in the intestinal barrier dysfunction and gut microbiota dysbiosis. In addition, intervention with L. casei ATCC 393, VIP or L. casei ATCC 393 combined with VIP significantly reduced UC disease activity index. However, compared with L. casei ATCC 393 or VIP, L. casei ATCC 393 combined with VIP effectively relieved symptoms of UC by regulating immune response, enhancing antioxidant capacity, and regulating nuclear factor kappa-B (NF-κB) and nuclear factor erythroid-derived-2-like 2 (Nrf2) signaling pathways. In conclusion, this study suggests that L. casei ATCC 393 combined with VIP can effectively relieve DSS-induced UC, which is a promising treatment strategy for UC.

Biogenic selenium nanoparticles alleviate intestinal epithelial barrier injury by regulating mitochondria-lysosome crosstalk.

The intestinal epithelial barrier plays a fundamental role in human and animal health. Mitochondrial dysfunction can lead to intestinal epithelial barrier damage. The interaction between mitochondria and lysosomes has been proved to regulate each other's dynamics. Our previous studies have demonstrated that biogenic selenium nanoparticles (SeNPs) can alleviate intestinal epithelial barrier injury through regulating mitochondrial autophagy. In this study, we hypothesize that the protective effects of SeNPs against intestinal epithelial barrier dysfunction are associated with mitochondrial-lysosomal crosstalk. The results showed that lipopolysaccharide (LPS) and TBC1D15 siRNA transfection both caused the increase of intestinal epithelial permeability, activation of mitophagy, and mitochondrial and lysosomal dysfunction in porcine jejunal epithelial cells (IPEC-J2). SeNP pretreatment significantly up-regulated the expression levels of TBC1D15 and Fis1, down-regulated Rab7, caspase-3, MCOLN2 and cathepsin B expression levels, reduced cytoplasmic Ca2+ concentration, effectively alleviated mitochondrial and lysosomal dysfunction, and maintained the integrity of the intestinal epithelial barrier in IPEC-J2 cells exposed to LPS. Furthermore, SeNPs obviously reduced cytoplasmic Ca2+ concentration and activated the TBC1D15/Fis/Rab7-mediated signaling pathway, shortened the contact time between mitochondria and lysosomes, inhibited mitophagy, maintained mitochondrial and lysosomal homeostasis, and effectively attenuated intestinal epithelial barrier injury in IPEC-J2 cells transfected with TBC1D15 siRNA. These results indicated that the protective effect of SeNPs on intestinal epithelial barrier injury is closely associated with the TBC1D15/Rab7-mediated mitochondria-lysosome crosstalk signaling pathway.

Selenite Bioremediation by Food-Grade Probiotic Lactobacillus casei ATCC 393: Insights from Proteomics Analysis.

Microorganisms capable of converting toxic selenite into elemental selenium (Se0) are considered an important and effective approach for bioremediation of Se contamination. In this study, we investigated the mechanism of reducing selenite to Se0 and forming Se nanoparticles (SeNPs) by food-grade probiotic Lactobacillus casei ATCC 393 (L. casei ATCC 393) through proteomics analysis. The results showed that selenite added during the exponential growth period of bacteria has the highest reduction efficiency, and 4.0 mM selenite decreased by nearly 95% within 72 h and formed protein-capped-SeNPs. Proteomics analysis revealed that selenite induced a significant increase in the expression of glutaredoxin, oxidoreductase, and ATP binding cassette (ABC) transporter, which can transport glutathione (GSH) and selenite. Selenite treatment significantly increased the CydC and CydD (putative cysteine and glutathione importer, ABC transporter) mRNA expression level, GSH content, and GSH reductase activity. Furthermore, supplementation with an additional GSH significantly increased the reduction rate of selenite, while GSH depletion significantly inhibited the reduction of selenite, indicating that GSH-mediated Painter-type reaction may be the main pathway of selenite reduction in L. casei ATCC 393. Moreover, nitrate reductase also participates in the reduction process of selenite, but it is not the primary factor. Overall, L. casei ATCC 393 effectively reduced selenite to SeNPs by GSH and nitrate reductase-mediated reduction pathway, and the GSH pathway played the decisive role, which provides an environmentally friendly biocatalyst for the bioremediation of Se contamination. IMPORTANCE Due to the high solubility and bioavailability of selenite, and its widespread use in industrial and agricultural production, it is easy to cause selenite to accumulate in the environment and reach toxic levels. Although the bacteria screened from special environments have high selenite tolerance, their safety has not been fully verified. It is necessary to screen out strains with selenite-reducing ability from nonpathogenic, functionally known, and widely used strains. Herein, we found food-grade probiotic L. casei ATCC 393 effectively reduced selenite to SeNPs by GSH and nitrate reductase-mediated reduction pathway, which provides an environmentally friendly biocatalyst for the bioremediation of Se contamination.

Biogenic Selenium Nanoparticles Synthesized by Lactobacillus casei ATCC 393 Alleviate Acute Hypobaric Hypoxia-Induced Intestinal Barrier Dysfunction in C57BL/6 Mice.

Exposure to hypobaric hypoxia at high altitude will cause different tissue and organ damage over a long period of time. Studies have shown that hypobaric hypoxia can cause severe primary intestinal barrier dysfunction, and then cause multiple organ dysfunction. Our previous research showed that selenium nanoparticles (SeNPs) synthesized by Lactobacillus casei ATCC 393 (L. casei ATCC 393) can effectively alleviate intestinal barrier dysfunction caused by oxidative stress and inflammation in mice. This study was conducted to investigate the protective effect of biological SeNPs synthesized by L. casei ATCC 393 on intestinal barrier function in acute hypobaric hypoxic stress mice. The results showed that compared with the hypobaric hypoxic, the SeNPs synthesized by L. casei ATCC 393 by oral administration could effectively alleviate the shortening of intestinal villi, which decreased the level of diamine oxidase (DAO) and myeloperoxidase (MPO), and the expression level of tight junction protein in ileum was increased. In addition, SeNPs significantly increased the activities of superoxide dismutase (SOD), cyclooxygenase (COX-1) and glutathione peroxidase (GPx), and decreased the level of malondialdehyde (MDA), and inhibit the increase of hypoxia related factor. SeNPs effectively regulate the intestinal microecology disorder caused by hypobaric hypoxia stress, and maintain the intestinal microecology balance. In addition, oral administration of SeNPs had better protective effect on intestinal barrier function of mice under hypobaric hypoxia stress. These results suggested that SeNPs synthesized by L. casei ATCC 393 can effectively alleviate the damage of intestinal barrier function under acute hypobaric hypoxic stress, which may be closely related to the antioxidant activity of SeNPs.

Dietary supplementation with selenium nanoparticles-enriched Lactobacillus casei ATCC 393 alleviates intestinal barrier dysfunction of mice exposed to deoxynivalenol by regulating endoplasmic reticulum stress and gut microbiota.

Deoxynivalenol (DON), a secondary product of Fusarium metabolism, is common in wheat, corn, barley and other grain crops, posing a variety of adverse effects to environment, food safety, human and animal health. The absorption of DON mainly occurs in the proximal part of the small intestine, which can induce intestinal mucosal epithelial injury, and ultimately affect the growth performance and production performance of animals. This study was conducted to investigate the protective effects of selenium nanoparticles (SeNPs)-enriched Lactobacillus casei ATCC 393 (L. casei ATCC 393) on intestinal barrier function of C57BL/6 mice exposed to DON and its association with endoplasmic reticulum stress (ERS) and gut microbiota. The results showed that DON exposure increased the levels of interleukin-6 (IL-6) and interleukin-8 (IL-8), decreased the levels of interleukin-10 (IL-10) and transforming growth factor beta (TGF-ß), caused a redox imbalance and intestinal barrier dysfunction, decreased the mRNA levels of endoplasmic reticulum- resident selenoproteins, activated ERS-protein kinase R-like endoplasmic reticulum kinase (PERK) signaling pathway, altered the composition of the gut microbiota and decreased short-chain fatty acids (SCFAs) content. Dietary supplementation with SeNPs-enriched L. casei ATCC 393 can effectively protect the integrity of intestinal barrier function by reducing inflammatory response, enhancing the antioxidant capacity, up-regulating the mRNA levels of endoplasmic reticulum-resident selenoproteins, inhibiting the activation of PERK signaling pathway, reversing gut microbiota dysbiosis and increasing the content of SCFAs in mice exposed to DON. In conclusion, dietary supplementation with SeNPs-enriched L. casei ATCC 393 effectively alleviated intestinal barrier dysfunction induced by DON in C57BL/6 mice, which may be closely associated with the regulation of ERS and gut microbiota.

Protective effect of biogenic selenium nanoparticles against diquat-induced acute toxicity via regulation of gut microbiota and its metabolites.

Selenium nanoparticles (SeNPs) with unique biological properties have been suggested as a safer and more effective platform for delivering of Selenium for biological needs. In this study, we investigated the association between gut microbiota altered by SeNPs supplementation and its metabolites under oxidative stress conditions through 16S rDNA gene sequencing analysis and untargeted metabolomics. The results showed that dietary supplementation with SeNPs attenuated diquat-induced acute toxicity in mice, as demonstrated by lower levels of inflammatory effector cells, and biochemical markers in serum such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and lactate dehydrogenase (LDH). SeNPs also reversed the perturbed gut microbiota composition induced by diquat, decreased the Firmicutes/Bacteroidetes ratio, and increased the abundance of beneficial bacteria such as Akkermansia, Muribaculaceae, Bacteroides and Parabacteroides. Untargeted fecal metabolomics showed that SeNPs can regulate the production of steroids and steroid derivatives, organonitrogen compounds, pyridines and derivatives and other metabolites. Microbiome-metabolome correlation analysis suggested that Parabacteroides was the key bacteria for the SeNPs intervention, which might upregulate the levels of metabolites such as trimethaphan, emedastine, berberine, desoxycortone, tetrahydrocortisone. This study demonstrated that dietary SeNPs supplementation can extensively modulate the gut microbiota and its metabolism, thereby alleviating diquat-induced acute toxicity.

Biogenic Selenium Nanoparticles Alleviate Intestinal Epithelial Barrier Damage through Regulating Endoplasmic Reticulum Stress-Mediated Mitophagy.

The intestinal barrier plays a fundamental role in body health. Intracellular redox imbalance can trigger endoplasmic reticulum stress (ERS) and mitophagy, leading to intestinal barrier damage. Our previous studies demonstrated that mitophagy is closely associated with the protective effects of biogenic selenium nanoparticles (SeNPs) on intestinal epithelial barrier function. Thus, we hypothesize that ERS and mitophagy are likely involved in the regulatory effects of SeNPs on oxidative stress-induced intestinal epithelial barrier dysfunction. The results showed that oxidative stress or ERS caused the increase of intestinal epithelial permeability. SeNPs effectively alleviated hydrogen peroxide (H2O2-)-induced structural damage of endoplasmic reticulum (ER) and mitochondria of porcine jejunal epithelial cells (IPEC-J2). SeNPs significantly decreased intracellular inositol triphosphate (IP3) and Ca2+ concentration, down-regulated inositol trisphosphate receptor (IP3R) expression level, and up-regulated ER-resident selenoproteins mRNA levels in IPEC-J2 cells exposed to H2O2. In addition, SeNPs pretreatment significantly decreased the intracellular Ca2+, IP3, IP3R, and reactive oxygen species (ROS) levels; protected the structure and function of ER and mitochondria; and effectively alleviated the increase of intestinal epithelial permeability of IPEC-J2 cells exposed to tunicamycin (TM). Moreover, SeNPs significantly inhibited the colocalization of mitochondria and lysosomes. Furthermore, compared with TM model group, SeNPs significantly inhibited the activation of PERK/eIF2α/ATF4 and AMPK/mTOR/PINK1 signaling pathway. The PERK agonist (CCT020312) and the AMPK agonist (AICAR) could reverse the protective effects of SeNPs on IPEC-J2 cells. The PERK inhibitor (GSK2656157) and the AMPK inhibitor (compound C) had a similar effect on IPEC-J2 cells as that of SeNPs. In summary, the protective effects of SeNPs on intestinal barrier dysfunction are closely associated with ERS-related PERK and mitophagy-related AMPK signaling pathway.

Dietary supplementation with biogenic selenium nanoparticles alleviate oxidative stress-induced intestinal barrier dysfunction.

Selenium (Se) is an essential micronutrient that promotes body health. Endemic Se deficiency is a major nutritional challenge worldwide. The low toxicity, high bioavailability, and unique properties of biogenic Se nanoparticles (SeNPs) allow them to be used as a therapeutic drug and Se nutritional supplement. This study was conducted to investigate the regulatory effects of dietary SeNPs supplementation on the oxidative stress-induced intestinal barrier dysfunction and its association with mitochondrial function and gut microbiota in mice. The effects of dietary SeNPs on intestinal barrier function and antioxidant capacity and its correlation with gut microbiota were further evaluated by a fecal microbiota transplantation experiment. The results showed that Se deficiency caused a redox imbalance, increased the levels of pro-inflammatory cytokines, altered the composition of the gut microbiota, and impaired mitochondrial structure and function, and intestinal barrier injury. Exogenous supplementation with biogenic SeNPs effectively alleviated diquat-induced intestinal barrier dysfunction by enhancing the antioxidant capacity, inhibiting the overproduction of reactive oxygen species (ROS), preventing the impairment of mitochondrial structure and function, regulating the immune response, maintaining intestinal microbiota homeostasis by regulating nuclear factor (erythroid-derived-2)-like 2 (Nrf2)-mediated NLR family pyrin domain containing 3 (NLRP3) signaling pathway. In addition, Se deficiency resulted in a gut microbiota phenotype that is more susceptible to diquat-induced intestinal barrier dysfunction. Supranutritional SeNPs intake can optimize the gut microbiota to protect against intestinal dysfunctions. This study demonstrates that dietary supplementation of SeNPs can prevent oxidative stress-induced intestinal barrier dysfunction through its regulation of mitochondria and gut microbiota.

Lactobacillus casei ATCC 393 and it's metabolites alleviate dextran sulphate sodium-induced ulcerative colitis in mice through the NLRP3-(Caspase-1)/IL-1ß pathway.

Inflammatory bowel disease (IBD) represents a broad group of intestinal disorders, including ulcerative colitis (UC) and Crohn's disease (CD). Probiotics are increasingly being recognized as a means of treatment for people suffering from IBD. Our previous studies demonstrated that Lactobacillus casei ATCC 393 (L. casei ATCC 393) effectively alleviated enterotoxigenic Escherichia coli K88-induced intestinal barrier dysfunction. This study was conducted to investigate the protective effects of L. casei ATCC 393 and its metabolites on dextran sulfate sodium (DSS)-induced UC in C57BL/6 mice and the potential mechanism of these effects. The results showed that oral administration of L. casei ATCC 393 and its metabolites both effectively reversed the DSS-induced weight loss, and the reduction in the disease activity index (DAI), colon length, and villus height of colon tissue in mice. Compared to the DSS-induced model group, L. casei ATCC 393 and its metabolites significantly inhibited the infiltration of immune cells into the intestinal mucosa, decreased the production of pro-inflammatory factors, and increased the expression of anti-inflammatory factors in the serum and colon tissue, increased the expression levels of occludin, ZO-1, and claudin-1, and reduced the expression of nucleotide binding oligomeric domain-like receptor protein 3 (NLRP3), cysteine proteinase-1 (Caspase-1), IL-1ß, and IL-18. In addition, L. casei ATCC 393 and its metabolites effectively improved DSS-induced gut microbiota dysbiosis. These results suggested that L. casei ATCC 393 and its metabolites alleviated the DSS-induced ulcerative inflammatory response in C57BL/6 mice through the NLRP3-(Caspase-1)/IL-1ß signaling pathway.

Nitric Oxide Production Inhibitory Eudesmane-Type Sesquiterpenoids from Artemisia argyi.

Six new eudesmane-type sesquiterpene derivatives, artemargyinins A-F were isolated from the leaves of Artemisia argyi. Their structures were elucidated based on the extensive analysis of spectroscopic data. Artemargyinins A-F feature a lactone ring-opening eudesmane-type sesquiterpene with an isoprenoid group at C(8). All compounds were tested for their inhibitory effects on lipopolysaccharide-induced nitric oxide (NO) production in RAW264.7 macrophages. Artemargyinins A-F showed more potent NO production inhibitory activity with IC50 values ranging from 7.66±0.53 to 61.19±2.54 µM than the positive control quercetin (IC50 =74.34±1.39 µM). Among them, artemargyinins C and D exhibited strong inhibitory activity with IC50 values of 8.08±0.21 and 7.66±0.53 µM, respectively.

Triterpenoids with α-glucosidase inhibitory activity from Artemisia argyi.

Two new nordammarane-type triterpenoids, 3ß-acetoxy-20-oxo-21-nordammaran-23-carboxylic acid methyl ester (1) and 3ß-acetoxy-17ß-dammaranic acid (2), along with two known cycloartane-type triterpenoids (3-4), were isolated from the petroleum ether-soluble extract of Artemisia argyi. Their structures were elucidated based on 1D and 2D NMR spectroscopic data analysis. All compounds were evaluated for their α-glucosidase inhibitory activity in vitro. Compounds 1-4 exhibited significant inhibitory effects on α-glucosidase with IC50 values ranging from 38.34 ± 0.23 to 105.54 ± 0.33 µM.