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This study aimed to examine the potential impact of the intervention of Lactiplantibacillus plantatum HFY11 (LP-HFY11) on colitis using in vivo animal trials. The impact of LP-HFY11 intervention on colitis was determined by measuring the levels of relevant indicators in the intestine, colon, and blood after oxazolone-induced colitis in BALB/c mice. The results of the trial show that LP-HFY11 improved the colon weight-to-length ratio, reduced the colitis-induced colon length shortening, and reduced colonic abstinence. Furthermore, it decreased the levels of myeloperoxidase, nitric oxide, and malondialdehyde activities while increasing the glutathione content in the colon tissue of colitis-affected animals. LP-HFY11 lowered the interleukin-10 (IL-10) level and increased the IL-2 level in the serum of colitis mice. LP-HFY11 also upregulated the expression of neuronal nitric oxide synthase, endothelial nitric oxide synthase, c-Kit, and stem cell factor (SCF), and downregulated the expression of IL-8, C-X-C chemokine receptor type 2 (CXCR2), and inducible nitric oxide synthase (iNOS) in the colon tissue of mice with colitis. LP-HFY11 decreased the expression of Firmicutes in the gut while increasing the expression of Bacteroidetes, Bifidobacteria, and Lactobacillus. This indicates that LP-HFY11 could control physiological alterations in the serum and colon tissue, as well as the expression of gut microorganism. [ABSTRACT FROM AUTHOR]

Gonggan (Citrus reticulata Blanco var. gonggan) is one of the most popular citruses. In this study, the effect of Gonggan peel extract (GPE) on gastric injury was investigated. The components in GPE were analysed by HPLC and the gastric injury model in mice was established by ethanol/hydrochloric acid. After treatment by GPE, the pathological changes of gastric tissue were observed by optical microscope. The levels of oxidative stress and inflammation were measure by kit. And the mRNA expression of related gene was determined by qPCR assay. HPLC result showed GPE mainly contained the flavonoids narirutin, hesperidin, nobiletin, tangeretin and 5-demethylnobiletin. Morphological and pathological analysis of gastric tissue revealed that GPE could relieve gastric injury. Also, GPE increased the levels of SOD, GSH-Px, and CAT and decreased the level of MDA. Moreover, GPE decreased the levels of the inflammatory cytokines TNF-α, IFN-γ, IL-1β, and IL-6 to suppress inflammation. In addition, the q-PCR results showed that GPE upregulated the mRNA expression of SOD1, SOD2, γ-GCS, GSH-Px, CAT, and IκBα and downregulated the mRNA expression of NF-κB. In conclusion, GPE alleviated gastric injury caused by ethanol/hydrochloric acid by inhibiting oxidative stress and the inflammatory response. The mechanism by which GPE protects gastric tissues may involve the antioxidative pathway. Therefore, GPE has great potential to be developed as a product to prevent gastric injury. [ABSTRACT FROM AUTHOR]

Insect tea is consumed as a health beverage in China. The insect tea primary leaf (ITPL) is rich in bioactive substances, which are also used as traditional Chinese medicine. This study investigated the role of ITPL in reducing the oxidative response induced by D‐galactose in mice. Mice were intraperitoneally injected with D‐galactose to induce oxidative damage. The effect of ITPL was tested by pathological observation, serum detection with kits, quantitative polymerase chain reaction, and Western blot. The experimental results show that ITPL increased the thymus, brain, heart, liver, spleen, and kidney indices of oxidized mice. ITPL increased superoxide dismutase, glutathione peroxidase, and glutathione levels and reduced nitric oxide and malondialdehyde levels in the serum, liver, and spleen in oxidative damaged mice. The pathological observations show that ITPL reduced the oxidative damage of the liver and spleen in mice induced with D‐galactose. Simultaneously, ITPL upregulated mRNA expression of neuronal nitric oxide synthase, endothelial nitric oxide synthase, cuprozinc‐superoxide dismutase, manganese superoxide dismutase, catalase, heme oxygenase‐1, nuclear factor‐erythroid 2 related factor 2, γ‐glutamylcysteine synthetase, and NAD(P)H dehydrogenase [quinone] 1, and downregulated the expression of inducible nitric oxide synthase in the liver and spleen of oxidized mice. ITPL had beneficial preventive effects on the oxidative damage caused by D‐galactose in mice and was more effective as an antioxidant than vitamin C. The component analysis test by high‐performance liquid chromatography indicated that ITPL contained the following seven compounds: neochlorogenic acid, cryptochlorogenic acid, rutin, kaempferin, isochlorogenic acid B, isochlorogenic acid A, and hesperidin. ITPL is a plant with excellent antioxidant activities derived from its bioactive substances. [ABSTRACT FROM AUTHOR]

In the present research, the effects of Lactobacillus plantarum YS4 (LP-YS4) on colitis were tested in an oxazolone-induced mouse model. BALB/c mice were induced by oxazolone and then treated with LP-YS4. The serum levels of mice were analyzed using commercial kits and the protein and mRNA expression levels of mouse colon tissue were detected by Western blotting and qPCR assay, respectively. The results demonstrated that LP-YS4 significantly (P < 0.05) increased the colon length and ratio of colon weight/length in mice with colitis and attenuated the negative effects of colitis. The results also showed that treatment with LP-YS4 significantly reduced the serum concentrations of ET-1, SP, and IL-10 while significantly increasing those of SS, VIP, and IL-2 in colitis mice (P < 0.05). In addition, LP-YS4 significantly increased the activities of GSH and SOD while decreasing those of MPO and MDA in the colon tissue of colitis mice (P < 0.05). LP-YS4 also significantly upregulated the mRNA and protein expression of c-Kit, eNOS, nNOSe, and SCF in colitis mice while significantly downregulating the relative expression of iNOS. In summary, LP-YS4 could reduce the negative effects of colitis, and such effects were better than those of the common probiotic Lactobacillus bulgaricus. [ABSTRACT FROM AUTHOR]

Yogurt from Xinjiang, China, is a traditional Chinese fermented food rich in beneficial microorganisms, such as Lactobacillus plantarum KSFY06. In this study, the effect of KSFY06 on oxidative aging was investigated using live animal experiments. Molecular biological methods were used to analyze the serum and tissues of mice with oxidative aging induced by d‐galactose, which showed that KSFY06 can inhibit the decline of heart, liver, spleen, and kidney caused by aging. The KSFY06 strain increased the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), catalase (CAT), and glutathione (GSH) in serum and liver of aging mice, while the content of malondialdehyde (MDA) is reduced. Pathological observation showed that KSFY06 alleviated damage to the liver, spleen, and skin of oxidative aging mice. qPCR showed that, at high dose (2 × 109 cfu/kg per day), KSFY06 upregulates copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS), catalase (CAT) mRNA expression, and its downstream inducible nitric oxide synthase (iNOS) mRNA expression in liver and spleen tissues induced by d‐gal. To a certain extent, these findings indicate that L. plantarum KSFY06 is able to protect against oxidative stress in the d‐gal‐induced aging model. In conclusion, L. plantarum KSFY06 may provide a potential research value in the prevention or alleviation of related diseases caused by oxidative stress. [ABSTRACT FROM AUTHOR]

Insect tea is a traditional Chinese drink that contains abundant bioactive substances. In this study, the preventive effect of Insect tea on D‐galactose‐induced oxidation in mice was studied. The serum, liver, and spleen of mice were measured by biochemical and molecular biological methods, which showed that Insect tea could increase the biochemical indexes of the thymus, brain, heart, liver, spleen, and kidney in mice with induced oxidative damage. Insect tea can increase the levels of SOD (superoxide dismutase), GSH‐Px (glutathione peroxidase), and GSH (glutathione) and decrease the levels of MDA (malondialdehyde) in the serum, liver, and spleen of mice with oxidative damage. Pathological observation also confirmed that Insect tea could inhibit oxidative damage of the liver and spleen tissue caused by D‐galactose in mice. Further molecular biological experiments also showed that Insect tea could upregulate the mRNA and protein expression of Cu/Zn‐SOD (cuprozinc‐superoxide dismutase), Mn‐SOD (manganese superoxide dismutase), CAT (catalase), HO‐1 (heme oxygenase‐1), Nrf2 (nuclear factor‐erythroid 2 related factor 2), γ‐GCS (γ‐glutamylcysteine synthetase), and NQO1 (NAD(P)H dehydrogenase [quinone] 1) in the liver and spleen of oxidized mice. Insect tea has a good preventive effect on D‐galactose‐induced oxidation in mice, and the effect is better than vitamin C, an antioxidant. Insect tea is rich in isochlorogenic acid A, quercetin, rutin, hesperidin, neochlorogenic acid, and cryptochlorogenic acid. The combination of these bioactive substances has good antioxidant effects. Thus, Insect tea is a functional food with a good antioxidant effect that has value for future development and utilization. [ABSTRACT FROM AUTHOR]

In this study, the effect of lotus leaf flavonoids (LLF) on carbon tetrachloride (CCl4)-induced liver injury in mice was studied. CCl4 was injected intraperitoneally to induce liver injury in Kunming mice. Mice were treated with LLF by gavage, and the mRNA expression levels in serum and liver were detected. Compared with the model group, LLF significantly reduced the liver index and serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), and total cholesterol (TC) levels in mice with CCl4-induced liver injury. Pathological observation showed that LLF effectively reduced morphological incompleteness and hepatocyte necrosis in CCl4-treated liver tissue. The result of quantitative polymerase chain reaction (qPCR) indicated that LLF significantly up-regulated the mRNA expression levels of copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and catalase (CAT) and down- regulated the expression levels of tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), and interleukin-1β (IL-1β) (p < 0.05). Thus, LLF is an active ingredient that ameliorates liver injury, and it has good application prospect. [ABSTRACT FROM AUTHOR]

Yak yogurt is a type of naturally fermented dairy product prepared by herdsmen in the Qinghai-Tibet Plateau, which is rich in microorganisms. In this study, a strain of Lactobacillus plantarum was isolated and identified from yak yogurt in Hongyuan, Sichuan Province and named Lactobacillus plantarum HFY05 (LP-HFY05). LP-HFY05 was compared with a common commercial strain of Lactobacillus delbrueckii subsp. bulgaricus (LDSB). LP-HFY05 showed better anti-artificial gastric acid and bile salt effects than LDSB in in vitro experiments, indicating its potential as a probiotic. In animal experiments, long-term alcohol gavage induced alcoholic liver injury. LP-HFY05 effectively reduced the liver index of mice with liver injury, downregulated the levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triglyceride, total cholesterol, blood urea nitrogen, nitric oxide, and MDA and upregulated the levels of albumin, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase in the serum of liver-injured mice. LP-HFY05 also reduced the levels of interleukin (IL)-6, IL-12, tumor necrosis factor-alpha, and interferon-gamma in the serum of liver-injured mice. The pathological observations showed that LP-HFY05 reduced the damage to liver cells caused by alcohol. Quantitative polymerase chain reaction and Western blot assays further showed that LP-HFY05 upregulated neuronal nitric oxide synthase, endothelial nitric oxide synthase, manganese-SOD, cuprozinc-SOD, CAT, and inhibitor of κB-α mRNA and protein expression and downregulated the expression of nuclear factor-κB-p65 and inducible nitric oxide synthase in the livers of liver-injured mice. A fecal analysis revealed that LP-HFY05 regulated the microbial content in the intestinal tract of mice with liver injury, increased the content of beneficial bacteria, including Bacteroides, Bifidobacterium, and Lactobacillus and reduced the content of harmful bacteria, including Firmicutes, Actinobacteria, Proteobacteria, and Enterobacteriaceae, thus, regulating intestinal microorganisms to protect against liver injury. The effect of LP-HFY05 on liver-injured mice was better than that of LDSB, and the effect was similar to that of silymarin. LP-HFY05 is a high-quality microbial strain with a liver protective effect on experimental mice with alcoholic liver injury. [ABSTRACT FROM AUTHOR]

As a traditional Chinese medicinal drink, Apocynum venetum, a local tea from Xinjiang, China, is favored for its rich flavor and biological functionality. This study looked at aging mice induced by d-galactose to determine the in vivo anti-aging effect of Apocynum venetum tea extracts (AVTEs) and its bioactive components. We evaluated the weight of major organs (via organ index) and pathological changes in the liver. We also detailed the effects of AVTE (250 mg/kg in the low dose group, 500 mg/kg in the high dose group) on biochemical parameters (malondialdehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase, total antioxidant capacity, and nitric oxide) and cytokines (IL-6, IL-12, TNF-α and IL-1β) in the serum of aging mice. We investigated the anti-aging effects of AVTE in d-galactose-induced aging mice via quantitative real-time reverse transcription-polymerase chain reaction (RT-qPCR) assay. In addition, we analyzed the biological components of AVTEs by high performance liquid chromatography (HPLC). The results were remarkable, suggesting that AVTE significantly improved d-galactose-induced aging mice, with the high dose group showing the best results among other groups. ATVE can effectively alleviate hepatocyte edema, as well as inflammatory cell infiltration and injury in mice, induce a protective effect via up-regulation of glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) antioxidant related factors, and play an important role in the up-regulation of anti-inflammatory factors (IL-10) and the down-regulation of pro-inflammatory factors (IL-6, TNF-α and IL-1β). At the same time, HPLC analysis showed that AVTEs contain neochlorogenic acid, chlorogenic acid, cryptochlorogenic acid, rutin, isoquercitrin, isochlorogenic acid B, isochlorogenic acid A, astragalin, isochlorogenic acid C, rosmarinic acid, and trans-cinnamic acid. Thus, AVTE appears to be an effectively functional drink due to its rich functional components and anti-aging activities. [ABSTRACT FROM AUTHOR]

Sichuan pickle is a traditional fermented food in China which is produced by the spontaneous fermentation of Chinese cabbage. In this study, the anti-obesity effects of a new lactic acid bacterium (Lactobacillus fermentum CQPC05, LF-CQPC05) isolated from Sichuan pickles were assessed in vivo. An obese animal model was established in mice by inducing obesity with high-fat diet. Both serum and tissues were collected from the mice, and then subjected to qPCR and Western blot analyses. The results showed that LF-CQPC05 could decrease the values of hepatosomatic, epididymal fat, and perirenal fat indices that were induced by a high-fat diet in mice. Moreover, LF-CQPC05 reduced the levels of alanine aminotransferase (ALT), aspartate aminotransaminase (AST), total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C), and increased the level of high-density lipoprotein cholesterol (HDL-C) in both serum samples and liver tissues of obese mice fed with a high-fat diet. Pathological observations demonstrated that LF-CQPC05 could alleviate the obesity-induced pathological changes in the liver tissue of mice, and reduce the degree of adipocyte enlargement. The results of qPCR and Western blot analyses further indicated that LF-CQPC05 upregulated the mRNA and protein expression levels of lipoprotein lipase (LPL), PPAR-α: peroxisome proliferator-activated receptor-alpha (PPAR-α), (cholesterol 7 alpha-hydroxylase) CYP7A1, and carnitine palmitoyltransferase 1 (CPT1A), and downregulated the expression levels of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and CCAAT enhancer-binding protein alpha (C/EBP-α) in both liver tissue and epididymal adipose tissue. Taken altogether, this study reveals that LF-CQPC05 can effectively inhibit high-fat diet-induced obesity. Its anti-obesity effect is comparable to that of l-carnitine, and is superior to that of Lactobacillus delbrueckii subsp. bulgaricus, a common strain used in the dairy industry. Therefore, LF-CQPC05 is a high-quality microbial strain with probiotic potential. [ABSTRACT FROM AUTHOR]

The prevention and treatment of acute chest syndrome (ACS) is a major clinical concern in sickle cell disease (SCD). However, the mechanism underlying the pathogenesis of ACS remains elusive. We tested the hypothesis that the hemolysis byproduct hemin elicits events that induce ACS. Infusion of a low dose of hemin caused acute intravascular hemolysis and autoamplification of extracellular hemin in transgenic sickle mice, but not in sickle-trait littermates. The sickle mice developed multiple symptoms typical of ACS and succumbed rapidly. Pharmacologic inhibition of TLR4 and hemopexin replacement therapy prior to hemin infusion protected sickle mice from developing ACS. Replication of the ACS-like phenotype in nonsickle mice revealed that the mechanism of lung injury due to extracellular hemin is independent of SCD. Using genetic and bone marrow chimeric tools, we confirmed that TLR4 expressed in nonhematopoietic vascular tissues mediated this lethal type of acute lung injury. Respiratory failure was averted after the onset of ACS-like symptoms in sickle mice by treating them with recombinant hemopexin. Our results reveal a mechanism that helps to explain the pathogenesis of ACS, and we provide proof of principle for therapeutic strategies to prevent and treat this condition in mice. [ABSTRACT FROM AUTHOR]