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In this research, the differences in protein and fatty acid composition among camel, cow and goat milks were analyzed by gel electrophoresis (GE) and gas chromatography (GC). The GE results showed that there were differences in the proportion of proteins in camel milk from different regions, and the production process had a significant effect on both camel milk protein and milk fat globule membrane protein composition. There were significant differences in protein composition among camel, cow and goat milks, and camel milk did not contain β-lacglobulin or αs1-casein, while cow and goat milks did not contain immunoglobulin G2 (IgG2) or IgG3. Therefore, GE could be used for the identification of camel milk mixed with cow or goat milk. The GC results showed that 31 fatty acids were detected in both camel and goat milks, and 29 fatty acids in cow milk. Camel milk contained fewer short-chain fatty acids than cow and goat milks, while the contents of most long-chain fatty acids were significantly higher than those in cow and goat milks. Principal component analysis (PCA) of the fatty acid composition data showed a clear separation of milks from different species and a clear discrimination between pure and adulterated camel milk. PCA can be used for the identification and analysis of fatty acids in camel milk mixed with cow milk and goat milk.

Background: The prevalence of Hemagglutinin 9 Neuraminidase 2 (H9N2) avian influenza virus (AIV) in poultry in Asia has raised serious concerns about its zoonotic transmission and the potential for a pandemic, underscoring the need for effective therapeutics. Chikusetsusaponin IVa (CHS), a bioactive triterpenoid saponin from Radix saposhnikoviae, has exhibited anti-inflammatory activity in preclinical studies. We hypothesized that CHS could mitigate immunopathology during tumor necrosis factor (TNF)-infection by suppressing excessive inflammation. Objectives: CHS is a natural saponin with anti-inflammatory activity. This research aimed to explore the in vitro and in vivo protective effects and mechanisms of CHS against H9N2 AIV infection. Materials and Methods: We employed Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Gene Ontology (GO) analysis for the prediction of the underlying mechanisms, followed by a network analysis approach. In animal experiments, the toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathways and associated proteins were assessed using immunohistochemistry and western blot analysis. Results: In A549 cells, CHS treatment reduced H9N2 AIV-induced apoptosis in a dose-dependent manner. CHS was found to have a suppressive effect on the mRNA expression of various inflammatory cytokines (including TNF-α, interleukin (IL)-6, IL-1β, and IL-8) as well as mediators such as inducible nitric oxide synthase (iNOS) and prostaglandin-endoperoxide synthase 2 (PTGS2). It can be seen that CHS does have anti-inflammatory effects. Bioinformatics analysis indicated that CHS might exhibit anti-inflammatory effects by modulating cytokine–cytokine receptor interaction and the NF-κB signaling pathways. Building upon this, it was found that CHS blocked the activation of TLR4 and NF-κB signaling pathways in A549 cells infected with H9N2 AIV. In vivo, CHS prolonged the survival time and increased the survival rate of H9N2 AIV-infected mice. CHS was found to have a protective effect on the lungs of infected mice, resulting in reduced damage and lower levels of viral load and inflammation. CHS inhibited the production of proinflammatory cytokines (IL-1β, TNF-α, IL-6, and IL-8) and inhibited the activation of TLR4 and NF-κB signaling pathways in the pulmonary tissues of mice that were infected. Conclusion: CHS exerts protective effects against H9N2 AIV infection in vitro and in vivo. The anti-inflammatory mechanisms may involve the inhibition of cytokine production and the blockade of TLR4 and NF-κB signaling pathways. [ABSTRACT FROM AUTHOR]

Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a common troublesome side effect and affects long-term activities of daily living. This neuropathic disorder is still difficult to treat with current clinical treatments. The aim of this study was to investigate and offer an updated perspective of complementary therapies for CIPN.Methods: This review included current databases, including PubMed, Embase, the Cochrane Database, Google Scholar, and Ovid Medline, published up to May 2019 in the English language, to summarize the role of nutrient supplements in CIPN, based on evidence from both animal and clinical studies.Results: A total of 58 studies were included in this review. There were 19 preclinical studies that reported mechanisms of effects and 31 clinical studies corroborated preclinical findings, including 22 randomized controlled trials and 3085 patients with CIPN. Interventions included vitamin E, vitamin B complex, glutamine, acetyl-L-carnitine, alpha lipoic acid, glutathione, omega-3 fatty acids, and calcium/magnesium (Ca2+/Mg2+). The administration of various nutrients remains inconsistent, and limited evidence of effective ones for treating CIPN is available. However, glutamine and omega-3 fatty acids present potential as treatment options for CIPN. The evidence on vitamin E and vitamin B complex is inconclusive, and some forms of vitamin B, such as B6 or B12, await confirmation of their potential to offer protection from CIPN. Less robust evidence was found for nutrients such as acetyl-L-carnitine, α-Lipoic acid, glutathione, and Ca2+/Mg2+ for CIPN.Conclusion: Nutritional therapists seem to recommend nutrient supplements as potential anti-inflammatory and neuroprotective agents for both the prevention and management of CIPN. An understanding of this evolving literature is useful in exploring these therapies with patients who are considering using them. However, their effects against CIPN are still controversial due to the undetermined neuropathic mechanisms of different antineoplastic agents and complex drug interactions. Further research on these agents is warranted. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effect of Poria cocos (Schw.) Wolf hydroethanolic extract (PHE) against nephrotic syndrome (NS) in rats and to identify the potential active components from PHE. Methods: The high content compounds were isolated and purified by using column chromatography followed by preparative highperformance liquid chromatography (p-HPLC). Forty male Wistar rats with adriamycin (ADR)-induced NS were randomly divided into 5 groups, 8 in each group: model control group, positive control group (with prednisone treatment), PHE low-dose group, PHE middle-dose group and PHE high-dose group. Another 8 rats were recruited as vehicle control group. All rats received the intragastric administration of corresponding drugs or saline for 30 days. During the experimental period, rats' behavior and appearance were observed and recorded daily, and their body weights were recorded weekly. After treatment, 24-h urine samples were collected to evaluate the urine protein and urine creatinine (Ucr); then the rats were sacrificed to collect carotid blood and to determine the levels of serum total protein (TP), albumin (Alb), globulin (Glo), total cholesterol (TC) and cytokine interlukin-4 (IL-4). Results: Six acidic components were isolated and identified from the PHE section: pachymic acid, 15α-hydroxydehydrotumulosic acid, trametenolic acid, dehydropachymic acid, 3β-hydroxy-lanosta-7,9(11), 24-trien-21-oic-acid and dehydroeburicoic acid. Compared with the model control group, the urine protein content were significantly decreased in the PHE treatment groups and positive control group ( P<0.05), especially PHE middle-dose group ( P<0.01). The Ucr values and serum levels of TP, Glo, TC and IL-4 in PHE low- and middle-dose groups were also presented obvious recover tendency as compared with the model control group ( P<0.05 or P<0.01). However, positive control group and all PHE groups indicated no significant therapeutic effect on raising Alb value, although PHE low- and middle-dose treatment groups showed better outcomes than positive control group ( P>0.05). Conclusions: PHE showed an encouraging therapeutic effect against ADR-induced NS in a rat model. PHE might be a group of effective substances for the treatment of NS. [ABSTRACT FROM AUTHOR]