The integrity and permeability of the intestinal epithelial barrier are important indicators of intestinal health. Impaired intestinal epithelial barrier function and increased intestinal permeability are closely linked to the onset and progression of various intestinal diseases. Sinapic acid (SA) is a phenolic acid that has anti‐inflammatory, antihyperglycemic, and antioxidant activities; meanwhile, it is also effective in the protection of inflammatory bowel disease (IBD), but the specific mechanisms remain unclear. Here, we evaluated the anti‐inflammatory of SA and investigated its potential therapeutic activity in LPS‐induced intestinal epithelial barrier and tight junction (TJ) protein dysfunction. SA improved cell viability; attenuated epithelial permeability; restored the protein and mRNA expression of claudin‐1, ZO‐1, and occludin; and reversed the redistribution of the ZO‐1 and claudin‐1 proteins in LPS‐treated Caco‐2 cells. Moreover, SA reduced the inflammatory response by downregulating the activation of the TLR4/NF‐κB pathway and attenuated LPS‐induced intestinal barrier dysfunction by decreasing the activation of the MLCK/MLC pathway. This study demonstrated that SA has strong anti‐inflammatory activity and can alleviate the occurrence of high intercellular permeability in Caco‐2 cells exposed to LPS.

Ulcerative colitis is a chronic gastrointestinal disease characterized by intestinal inflammation and serious mucosal damage. As a naturally hydroxycinnamic acid, sinapic acid (SA) has antioxidant, anticancer, and neuroprotective activities. We investigated the anticolitic effect and potential mechanisms of SA in DSS-induced colitis in Kunming (KM) mice. SA treatment significantly reduced body weight loss, colon shortening, and intestinal wall thickening in colitis mice. SA treatment also significantly reduced the histological infiltration of inflammatory cells and decreased myeloperoxidase (MPO) activity in the colons of colitis mice. The administration of SA attenuated oxidative damage by enhancing the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase and reduced the serum and colonic mRNA levels of proinflammatory cytokines in colitis mice. We used qRT-PCR and Western blotting assays and demonstrated that SA reduced the activation of the NLRP3 inflammasome and attenuated intestinal permeability by enhancing the expression of ZO-1, occludin, and claudin-1 in colitis mice. Here, we conclude that SA exhibits great anticolitic activity against DSS-induced colitis by enhancing the activity of antioxidant enzymes, reducing intestinal inflammation, and maintaining the intestinal barrier. Finally, we suggest that SA may be a safe adjuvant for the prevention of clinical colitis.

Kudingcha is a traditional Chinese tea, and insect tea is a special drink produced by the metabolism of insect larvae using the raw Kuding tea. Insect tea polyphenols (ITP) and its raw tea (Kuding tea) polyphenols (KTP) are high-purity polyphenols extracted by centrifuge precipitation. The present study was designed to compare the antioxidative effects of insect tea polyphenols (ITP) and its raw tea (Kuding tea) polyphenols (KTP) on d-galactose-induced oxidation in Kunming (KM) mice. KM mice were treated with ITP (200 mg/kg) and KTP (200 mg/kg) by gavage, and vitamin C (VC, 200 mg/kg) was also used as a positive control by gavage. After determination in serum, liver and spleen, ITP-treated mice showed higher superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) activities and lower nitric oxide (NO), malonaldehyde (MDA) activities than VC-treated mice, KTP-treated mice and untreated oxidation mice (control group). By H&E section observation, the mice induced by d-galactose-induced oxidation showed more changes than normal mice, and oxidative damage appeared in liver and spleen tissues; ITP, VC and KTP improved oxidative damage of liver and spleen tissues, and the effects of ITP were better than VC and KTP. Using quantitative polymerase chain reaction (qPCR) and western blot experiments, it was observed that ITP could increase the mRNA and protein expression of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), manganese superoxide dismutase (Mn-SOD), cupro/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT), heme oxygenase-1 (HO-1), nuclear factor erythroid 2 related factor 2 (Nrf2), gamma glutamylcysteine synthetase (γ-GCS), and NAD(P)H:quinone oxidoreductase 1 (NQO1) and reduce inducible nitric oxide synthase (iNOS) expression in liver and spleen tissues compared to the control group. These effects were stronger than for VC and KTP. Both ITP and KTP had good antioxidative effects, and after the transformation of insects, the effects of ITP were better than that of KTP and even better than VC. Thus, ITP can be used as an antioxidant and anti-ageing functional food.

Yogurt from Xinjiang, China, is a traditional and naturally fermented food, and abundant microorganisms are produced during its fermentation process. In this study, we carried out in vivo animal experiments to explore the effect of a newly isolated lactic acid bacterial strain, Lactobacillus plantarum KSFY02 (LP-KSFY02), on oxidative aging. We used d-galactose to induce oxidative aging in mice and analyzed the serum and tissues of those mice using molecular biology detection methods. The results showed that LP-KSFY02 could inhibit the decreases in the thymic, cerebral, cardiac, liver, spleen, and kidney indices of mice caused by oxidative aging. The LP-KSFY02 strain increased activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) and reduced levels of nitric oxide (NO) and malondialdehyde in the serum, liver, and spleen of the oxidative aging mice. Pathological observation demonstrated that LP-KSFY02 alleviated damage to the liver and spleen of oxidative aging mice. Quantitative PCR showed that LP-KSFY02 effectively upregulated mRNA expression of neuronal nitric oxide synthase (Nos1), endothelial nitric oxide synthase (Nos3), copper/zinc superoxide dismutase (Sod1), manganese superoxide dismutase (Sod2), catalase (Cat), heme oxygenase-1 (Hmox1), nuclear factor erythroid 2 related factor 2 (Nfe2l2), γ-glutamylcysteine synthetase (Gclm), and quinone oxidoreductase 1 (Nqo1) in mouse liver and spleen and downregulated expression of inducible nitric oxide synthase (Nos2). Western blot analysis revealed that LP-KSFY02 effectively upregulated protein expression of SOD1, SOD2, CAT, GSH1, and GSH2 in mouse liver and spleen tissues. Therefore, LP-KSFY02 can effectively prevent d-galactose-induced oxidative aging in mice. Its efficacy was superior to that of Lactobacillus delbrueckii ssp. bulgaricus (LDSB) and vitamin C, which are commonly used in the medical field as antioxidants. Thus, LP-KSFY02 is a high-quality strain with probiotic potential.

Polycystic ovary syndrome (PCOS) is a common endocrine‐related cause of infertility in women and has an unknown etiology. Studies have shown that rhamnocitrin (Rha) exhibits positive effects on the reproductive system. This study investigated Rha’s antifibrotic effects on PCOS rats and revealed its underlying mechanisms. Female SD rats were randomized into 4 groups (n = 8, each); the control group received tea oil by intraperitoneal injection and 1% w/v CMC by oral gavage; the PCOS group received letrozole (1 mg/kg); the PCOS+Rha group received letrozole and Rha (5 mg/kg); the PCOS+Met group received letrozole and Met (265 mg/kg) for 21 days. At the study end, Rha treatment restored letrozole‐induced alterations in the relative ovarian weights, body weight, and relative weights of uterine and visceral adipose tissues. Histological observation showed that Rha ameliorates ovarian structure and fibrosis in PCOS. Administration of Rha reduced letrozole‐induced metabolic dysfunction by ameliorating the levels of TC, TG, and HDL‐C in the PCOS rats. Rha treatment also modulated the serum levels of sex hormones, which decreased T, E2, and LH and increased FSH in PCOS rats. In addition, Rha treatment modulated insulin resistance and increased gene expression of antioxidant enzymes (Cat, Sod2, Gpx3, Mgst1, Prdx3, Gsta4, Gsr, and Sod1) in the ovaries of the PCOS rats. Finally, Rha treatment appeared to increase the activity of PPAR‐γ and inhibit the TGF‐β1/Smad pathway in the ovaries of the PCOS rats. Our findings suggest that Rha significantly ameliorated metabolic disturbances and ovarian fibrosis in the PCOS rats. Rha perhaps is an effective compound for preventing ovarian fibrosis in the future.