Salidroside alleviates dextran sulfate sodium-induced colitis in mice by modulating the gut microbiota.

Dysbiosis causes continuous progress of inflammatory bowel disease (IBD). Herein, we aim to explore whether Salidroside (Sal), which is a major glycoside extracted from Rhodiola rosea L., could ameliorate dextran sulfate sodium (DSS)-induced colitis by modulating the microbiota. Results showed that oral treatment with 15 mg kg-1 of Sal inhibited DSS-induced colitis in mice as evidenced by colon length, histological analysis, disease activity index (DAI) score, and the proportion and number of macrophages in the intestine. The gut microbiota of colitic mice was also partly restored by Sal. A fecal microbiota transplantation (FMT) study was designed to verify the causality. Compared with DSS-treated mice, FM from the Sal-treated donor mice significantly mitigated the symptoms of colitic mice, including reducing the DAI score, alleviating tissue damage, boosting the expression of mucin protein (mucin-2) and tight junction (TJ) proteins (occludin and zonula occludens-1 (ZO-1), and decreasing M1 macrophages in the gut. It was found that both Sal and FMT affected the structure and abundance of the gut microbiota as reflected by the decreased relative abundance of Turicibacter, Alistipes, Romboutsia and the increased relative abundance of Lactobacillus at the genus level. Moreover, the anti-inflammatory effect of Sal disappeared when the gut microbiota was depleted by antibiotics, demonstrating that Sal alleviated the intestinal inflammation in a gut microbiota-dependent manner. Thus, Sal could be a remarkable candidate as a functional food for colitis.

Salidroside protects mice from high-fat diet-induced obesity by modulating the gut microbiota.

Obesity is a systemic disease with multisystem inflammation associated with gut dysbiosis. Salidroside (SAL) which is a major glycoside extracted from Rhodiola rosea L. has a wide range of pharmacological effects, but the role of gut microbiota in the protective effects of SAL on obesity has not been studied. Herein, we aim to explore whether SAL could ameliorate high-fat diet (HFD)-induced obesity in mice by modulating microbiota. Results showed that oral treatment with SAL alleviated HFD-induced obesity in mice as evidenced by body weight and fat weight. SAL supplementation effectively attenuated fat accumulation, lipid synthesis genes expression, liver inflammation, and metabolic endotoxemia. In addition, SAL treatment alleviated intestinal damage and increased the expression of mucin protein (Mucin-2) and tight junction (TJ) proteins (Occludin and Zonula Occludens-1). 16S rRNA sequencing analysis revealed that the gut microbiota of obese mice was also partly improved by SAL via restoring the microbial community structure and diversity. A fecal microbiota transplantation (FMT) study was designed to verify the causality. Compared with fecal transplantation (FM) from the HFD-treated mice, FM from the SAL-treated mice significantly mitigate the symptoms of obese mice, including decreasing body weight, fat accumulation, and attenuating pathological damage in the gut. Thus, SAL could be a remarkable candidate to prevent obesity.

Clostridium butyricum and Its Culture Supernatant Alleviate the Escherichia coli-Induced Endometritis in Mice.

Endometritis is a disease with a high incidence in dairy cows and causes great economic loss to milk production. This study examined the therapeutic effects of Clostridium butyricum and its culture supernatant on Escherichia coli-induced endometritis in mice. The results showed that Clostridium butyricum and its culture supernatant effectively suppressed inflammatory responses of uterine tissues, such as uterine morphological changes, pathological damage, and the production of inflammatory cytokines. Clostridium butyricum and its culture supernatant significantly decreased uterine microbial loads. In addition, Clostridium butyricum and its culture supernatant restored reproduction outcomes in Escherichia coli-induced endometritis mice. Western blot analysis showed that Clostridium butyricum and its culture supernatant suppressed the NF-κB signaling pathway. Therefore, the anti-inflammatory mechanism of Clostridium butyricum and its culture supernatant may occur through the anti-bacterial activity and regulation of the expression of NF-κB in the uterus. The anti-inflammatory effect of the culture supernatant of C. butyricum was slightly better than that of viable C. butyricum. Therefore, our experimental results showed that Clostridium butyricum culture supernatant may be an effective drug for treating endometritis.

Dioscin prevents DSS-induced colitis in mice with enhancing intestinal barrier function and reducing colon inflammation.

Dioscin is a natural steroid saponin derived from plants of the genus Dioscoreaceae. Previous studies have proved its effects of antibacterial, anti-inflammatory and hypolipidemic. In this study, our aim was to explore the protective effect and preliminary mechanism of Dioscin on dextran sulfate sodium (DSS)-induced colitis in mice. The results showed that Dioscin reduced DSS-induced disease activity index (DAI) increase, colon length shortening and colon pathological damage. In addition, Dioscin reduced excessive inflammation by reversing the cytokines levels, reducing intestinal macrophage infiltration and promoting macrophage polarization to M2 phenotype. At the same time, Dioscin maintained the intestinal barrier function by increasing the expression of zonula occludens-1 (ZO-1), occludin and mucin (Muc)-2. Moreover, Dioscin inhibited NF-κB, MAPK signaling and nucleotide oligomerization domain-like receptor family pyrin domain ontaining 3(NLRP3) inflammasome pathway in DSS-induced colitis. These results suggest that Dioscin is a competent candidate for ulcerative colitis (UC) therapy in the future.

The Abilities of Salidroside on Ameliorating Inflammation, Skewing the Imbalanced Nucleotide Oligomerization Domain-Like Receptor Family Pyrin Domain Containing 3/Autophagy, and Maintaining Intestinal Barrier Are Profitable in Colitis.

Salidroside (Sal), as a major glycoside extracted from Rhodiola rosea L., has exhibited its mighty anti-aging, anti-oxidant, anti-cancer, anti-inflammation, and neuroprotective effects in many diseases. Recently, it has showed its protective effect in colitis mice by activating the SIRT1/FoxOs pathway. Whereas, it is not known whether Sal has other protective mechanisms on dextran sulfate sodium (DSS)-induced colitis in mice. In this study, we investigated the protective effects and mechanisms of Sal on DSS-induced colitis in mice. The results demonstrated Sal was a competent candidate in the treatment of ulcerative colitis (UC). Sal remitted DSS-induced disease activity index (DAI), colon length shortening, and colonic pathological damage. Simultaneously, Sal alleviated excessive inflammation by reversing the IL-1ß, TNF-α, and IL-10 protein levels in DSS-treated mice. Western blot analysis revealed that Sal inhibited p65 and p38 activation together with peroxisome proliferator-activated receptor (PPARγ) up-regulation. In addition, Sal skewed the imbalanced activation of nucleotide oligomerization domain-like receptor family pyrin domain containing 3 inflammasome and autophagy contributing to colitis recovery. The damaged intestinal barrier induced by DSS was also alleviated along with plasma lipopolysaccharides (LPS) reduction after Sal treatment. In vitro, Sal showed PPARγ-dependent anti-inflammatory effect in LPS-stimulated RAW264.7 cells. In summary, our results demonstrated that Sal might be an effective factor for UC treatment and its pharmacological value deserved further development.

Protective Effect of Naringin on DSS-Induced Ulcerative Colitis in Mice.

Peroxisome proliferator-activated receptor γ (PPARγ) is an important member of the nuclear receptor superfamily. Previous studies have shown the satisfactory anti-inflammatory role of PPARγ in experimental colitis models, mainly through negatively regulating several transcription factors such as nuclear factor-κB (NF-κB). Therefore, regulating PPARγ and PPARγ-related pathways has great promise for treating ulcerative colitis (UC). In the present study, our objective was to explore the potential effect of naringin on dextran sulfate sodium (DSS) induced UC in mice and its involved potential mechanism. We found that naringin significantly relieved DSS-induced disease activities index (DAI), colon length shortening, and colonic pathological damage. Exploration of the potential mechanisms demonstrated that naringin significantly activated DSS-induced PPARγ and subsequently suppressed NF-κB activation. PPARγ inhibitor GW9662 largely abrogated the roles of naringin in vitro. Moreover, DSS induced the activation of mitogen-activated protein kinase (MAPK) and (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome was inhibited by naringin. Tight junction (TJ) architecture in naringin groups was also maintained by regulating zonula occludens-1 (ZO-1) expression. These results suggested that naringin may be a potential natural agent for protecting mice from DSS-induced UC.

Carbon footprint assessment for a local branded pure milk product: a lifecycle based approach

Abstract This paper provides a simplified life cycle based assessment for a local branded pure milk product, to measure its related carbon footprint, including production of raw milk, dairy processing, transportation of milk product and disposal of packaging waste. The results show that the total carbon footprint of the pure milk is 1120g CO2/L. The production of raw milk is identified as the major contributor to the carbon footprint. This contribution has amounted to 843 g of CO2 per liter of pure milk, accounted for 75.27% of the total carbon footprint. The carbon footprint of product transportation is 38 g of CO2 per liter, which accounts for 3.39% of the total. The carbon footprint related to the dairy processing and disposal of waste packaging is 173 g of CO2 per liter and 66 g of CO2 per liter, accounting for 15.45% and 5.89% of the total, respectively. The carbon footprint assessment intends to help dairy enterprises identify the intensive sectors of carbon emissions, and provides insight into improvement of product environmental performances.