The protective effects of walnut green husk polysaccharide on liver injury, vascular endothelial dysfunction and disorder of gut microbiota in high fructose-induced mice.

This study aimed to investigate the protective effects of walnut green husk polysaccharide (WGHP) on liver injury, vascular endothelial dysfunction and disorder of gut microbiota in mice induced by high fructose (HF) diet. The chemical analysis results show that the walnut green husk polysaccharide is a low molecular weight acidic heteropolysaccharide, composed mainly of glucuronic acid, arabinose and galactose. Biochemical analysis showed that WGHP significantly improved glucose metabolism and lipid metabolism and decreased oxidative stress in HF-diet induced obesity mice. Histopathological observation of liver and cardiovascular aorta confirmed the protective effects of WGHP on hepatic steatosis and vascular endothelial dysfunction. Furthermore, 16S rRNA sequencing results demonstrated that WGHP reversed the disorders of gut microbiota caused by HF, decreased the relative abundance of Verrucomicrobia and increased the relative abundance of Deferribacteres at the phylum level, decreased the relative abundance of Akkermansia, Lachnoclostridium and norank_f__Muribaculaceae and increased the relative abundance of Prevotellaceae_UCG-001, Helicobacter, Alloprevotella and Allobaculum at the genus levels. Our results indicate that WGHP may act as a functional polysaccharide for protecting liver and cardiovascular in HF-fed mice.

Kansuiphorin C and Kansuinin A ameliorate malignant ascites by modulating gut microbiota and related metabolic functions.

ETHNOPHARMACOLOGICAL RELEVANCE: Euphorbia kansui is a toxic Chinese herbal medicine and exhibits promising treatment to the malignant ascites (MA) in its traditional use. Ingenane-type and jastrophane-type diterpenes are demonstrated to be responsible for the toxicity and efficacy of kansui. Two representative compounds, kansuiphorin C (KPC) and kansuinin A (KA) in each type were proved to effectively reduce the ascites. The biological and toxicological effects are closely associated with the gastrointestinal tract, but the possible mechanism and related metabolic functions of KPC and KA treating MA through modulating the gut microbiota remain unclear. AIM OF THE STUDY: To investigate the possible mechanism and related metabolism of KPC and KA ameliorating malignant ascites through modulating gut microbiota. MATERIALS AND METHODS: MA rats and normal rats were divided into different groups and administrated with KPC, KA, and positive drug, respectively. 16S rDNA gene sequencing and metagenomes analysis combined with the quantification of short-chain fatty acids of feces were performed to reflect the modulation of gut microbiota. Then, the metabolites of KPC and KA in rat feces under the normal and pathological circumstances were detected by ultra-fast liquid chromatography coupled with MS/MS detector (UFLC-MS/MS) to explore the in-vivo bacterial biotransformation. RESULTS: KPC and KA were modulatory compounds for gut microbiota. The richness of Lactobacillus and the decreased abundance of Helicobacter involved in the carbohydrate metabolism and amino acid metabolism could be responsible for their prohibitory effects on malignant ascites. KPC exhibited stronger modulation of gut microbiota through making the abundance of Helicobacter about 3.5 times lower than KA. Besides, in-vivo microbial biotransformation of KPC and KA contained oxidation, hydrolysis, dehydration, and methylation to form metabolites of lower polarity. Besides, at the dosage of 10 mg kg-1, the toxicity of both compounds had weaker influences on the gut microbiota of normal rats. CONCLUSION: KPC and KA could ameliorate malignant ascites by modulating gut microbiota mainly containing the increase of Lactobacillus and the decrease of Helicobacter and related carbohydrate and amino acid metabolism, providing a basis for their promising clinical usage.

Helicobacter cinaedi bacteremia resulting from antimicrobial resistance acquired during treatment for X-linked agammaglobulinemia.

This is the first report of penicillin/cephalosporin-resistant Helicobacter cinaedi arising from prolonged treatment. H. cinaedi, common among immunocompromised patients, caused recurrent bacteremia and cellulitis in a 19-year-old Japanese man with X-linked agammaglobulinemia. The minimal inhibitory concentration of these drugs was raised, which subsequently resulted in clinical failure. Prolonged suboptimal treatment may cause bacterial resistance to ß-lactam antibiotics in H. cinaedi. It is possible that this resistance may have contributed to the treatment failure.

Utilização do óleo de alho e da amoxilina, metronidazol e omeprazol no controle de Helicobacter spp. em cães / Use of garlic oil and amoxicillin, metronidazole, and omeprazol in the control of Helicobacter spp. in dogs

Avaliaram-se a eficácia do óleo de alho e da terapia tripla (amoxicilina, metronidazol e omeprazol) no tratamento de 21 cães infectados por Helicobacter spp., que apresentavam alterações histológicas nas biopsias endoscópicas da mucosa gástrica e reação positiva ao teste de urease. Os animais foram distribuídos, aleatoriamente, em três grupos de sete cães, os quais receberam os seguintes tratamentos: grupo 1 - cápsulas vazias; grupo 2 - 500mg de óleo de alho em cápsulas, diariamente, por um período de 30 dias; grupo 3 - amoxicilina, metronidazol e omeprazol, respectivamente, nas doses de 20mg/kg a cada 12 horas, 25mg/kg e 20mg/kg a cada 24 horas, durante 15 dias. Ao final dos tratamentos, os cães foram submetidos à endoscopia com realização de biopsias da mucosa gástrica. O tratamento com amoxicilina, metronidazol e omeprazol resultou em erradicação de Helicobacter spp. tanto na região fúndica quanto na pilórica. No grupo 2, houve redução da degeneração glandular na região fúndica em dois animais e em outros dois na pilórica. O tratamento com óleo de alho não foi eficaz em erradicar Helicobacter spp., apenas reduziu a sua colonização em quatro dos animais tratados.

The efficacy of garlic oil and triple therapy (amoxicillin, metronidazole, and omeprazol) were evaluated in the treatment of 21 dogs infected by Helicobacter spp., which presented histological alterations of the gastric mucosa according to endoscopic biopsies and positive reaction to urease test. The animals were randomly distributed into three groups of seven dogs each, and received the following treatment, group 1 - empty capsules; group 2 - 500mg of garlic oil capsules daily for a period of 30 days; and group 3 - amoxicillin, metronidazole, and omeprazol, in doses of 20mg/kg every 12 hours, 25mg/kg and 20mg/kg every 24 hours, respectively, for 15 days. By the end of the treatment, the dogs were subjected to new endoscopic procedure with gastric mucosa biopsies. Treatment with amoxicillin, metronidazole, and omeprazol resulted in eradication of Helicobacter spp. both in fundic and pyloric regions. The garlic oil treatment reduced glandular degeneration in the fundic region in two animals and in the pylorus region in two other animals, and it was inefficient in eradicating Helicobacter spp. in dogs as it only reduced the colonization in some of the treated animals.

Long-term supplementation of canthaxanthin does not inhibit gastric epithelial cell proliferation in Helicobacter mustelae-infected ferrets.

The effect of canthaxanthin (CX), a nonprovitamin A carotenoid, on gastric epithelial proliferation was studied in ferrets colonized with Helicobacter mustelae, which causes a chronic gastritis and an increased gastric epithelial cell proliferation. Seven spayed female ferrets were dosed by gavage with CX beadlets (50 mg/kg body wt, 5 d/wk) over 2 y, whereas seven control animals were given placebo beadlets. At the end of the 2-y-period, ferrets were killed, and gastric tissues were obtained from the antrum and body regions. A cell-proliferating biomarker, proliferating cell nuclear antigen (PCNA), was assayed by immunohistochemistry. The PCNA positivity was measured by a computer-based image analysis system. Serum concentrations of carotenoids, retinoids and tocopherols were analyzed by HPLC. Serum antioxidant status was measured by the oxygen radical absorbance capacity (ORAC) assay. The PCNA positivity in both antrum and body regions was not significantly different between CX-fed ferrets and controls. Serum CX concentrations were significantly higher in CX-fed ferrets vs. controls (P < 0.001), whereas levels of other carotenoids, retinoids and tocopherols were not significantly different. The ORAC values were not significant different between groups. This study does not suggest inhibitory effects of CX on gastric epithelial cell proliferation in H. mustelae infected ferrets.