Hericium erinaceus is typically used in traditional Chinese medicine for mucosal protection, healing of gastric ulcers, and treatment of gastritis. We purified from the cultured mycelia of H. erinaceus a polysaccharide with anti-gastric ulcer and antigastritis activity, but its effects on gastric malignancy have not been elucidated. We examined the differential effects of this purified polysaccharide, named EP-1, on the human gastric (GES-1) cell line and a precancerous cell line (MC) that was transformed from GES-1 using N-methyl-N'-nitro-N-nitrosoguanidine. We observed that the polysaccharide potently induced cell apoptosis and cell cycle arrest at the G0/G1 phase in the MC cell line but did not have any effect on the GES-1 cell line at the same doses. Further mechanistic studies revealed that the polysaccharide exerted its activity through an apoptosis-associated pathway by modulating the expression of Bax, Bcl-2, and caspase-3. Differential effects of the polysaccharide on the GES-1 and MC cell lines indicate that the polysaccharide was effective in preventing gastric cancer progression.

In this study, the structure characteristic of the Hericium erinaceus polysaccharide (HEP) was investigated using Fourier transformed infrared spectrometry (FT-IR), gas chromatography-mass spectrometry (GC-MS), gel permeation chromatography (GPC), methylation and nuclear magnetic resonance (NMR). The results showed that HEP, with a molecular weight of 43 KDa, was mainly composed of glucose and rhamnose. The linkages of the sugar residues of HEP were → 6) β-d-Glcp-(1 → and → 2) -α-l-Rhap-(1 → residue at the end of the branches. The Fusarium toxin deoxynivalenol (DON)-induced cellular injury model for IPEC-J2 cells was established and used to investigate the protective effects of HEP against the oxidative stress. The results suggest that HEP could significantly protect IPEC-J2 cells from DON-induced oxidative stress, inhibit DON-induced apoptosis and reduce the production of reactive oxygen species (ROS). Overall, this study suggested that HEP could be explored as potential antioxidant agents for DON-induced intestinal mucosa injury.

Although cisplatin is a potent anticancer drug, it instigates oxidative and pro-inflammatory reactions which poses significant and distressing clinical symptoms in patients including nausea and vomiting which is related to damage of the gastric mucosa. This study investigated the effects of vitamin C and/or L-carnitine on cisplatin-induced gastric mucosa damage in rat. The rats were allocated into groups (n=5): a control group received distilled water and treatment groups received cisplatin (CIP) alone, cisplatin followed by vitamin C, L-carnitine or their combination. Cisplatin treatment caused disruption of the gastric mucosa histoarchitecture and alter the mucus barrier function in the gastric mucosa. Moreover, stomach tissue from the CIP treated group had increased levels of oxidative stress markers, malondialdehyde and H2O2 levels, and decreased activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, catalase, glutathione S-transferase and non-antioxidant enzyme, reduced glutathione level. These deleterious events were accompanied by upregulated levels of the pro-inflammatory cytokines, tumor necrosis factor-alpha, interleukin-1beta, and inflammatory infiltration markers, myeloperoxidase and inducible nitric oxide synthase (iNOS). However, administration of both vitamin C and L-carnitine, and not the either of the two showed additive effect in attenuating these toxic effects which were confirm histologically. In conclusion, the combined administration of vitamin C and L-carnitine, but not the single therapy, could prevent the adverse effects of cisplatin on gastric tissues.

Background. Electroacupuncture (EA) at ST36 has been used to regulate gastric motility and effectively improve gastric emptying in diabetic patients. Nevertheless, the specific mechanisms underlying the efficacy of this treatment remain unknown. The aim of this study was to assess the variations of interstitial cells of Cajal (ICC) and explore the changes in mSCF/KIT-ETV1 signaling in the antrum and corpus of diabetic mice after treatment with EA. Methods. Male C57BL/6 mice were randomized into five groups: control group, diabetic group (DM), diabetic-plus-sham EA group (SEA), diabetic-plus-low-frequency EA group (LEA), and diabetic-plus-high-frequency EA group (HEA). The expression levels of Ano1, c-Kit, and ETV1 were assessed by immunofluorescence in the antrum and corpus. Western blotting and PCR methods were further used to evaluate c-Kit, mSCF, and ETV1 expression. Results. (1) c-Kit and Ano1 were obviously decreased in the DM group, but c-Kit reduced much more than Ano1. (2) The mSCF, c-Kit, and ETV1 mRNA and protein levels were obviously decreased in the DM group in both the antrum and the corpus (P<0.01), but they were significantly elevated in the LEA and HEA groups (P<0.01). Conclusions. Ano1 is a reliable marker to detect ICC changes in diabetes; low- and high-frequency EA at acupoint ST36 can protect the networks of ICC possibly via normal activation of mSCF/KIT-ETV1 signaling.

The dietary pattern can influence the immune system directly, but may also modulate it indirectly by regulating the gut microbiota. Here, we investigated the effect of a 3-months lacto-ovo-vegetarian diet on the diversity of gut microbiota and the immune system in healthy omnivorous volunteers, using high-throughput sequencing technologies. The short-term vegetarian diet did not have any major effect on the diversity of the immune system and the overall composition of the metagenome. The prevalence of bacterial genera/species with known beneficial effects on the intestine, including butyrate-producers and probiotic species and the balance of autoimmune-related variable genes/families were, however, altered in the short-term vegetarians. A number of bacterial species that are associated with the expression level of IgA, a key immunoglobulin class that protects the gastrointestinal mucosal system, were also identified. Furthermore, a lower diversity of T-cell repertoire and expression level of IgE, as well as a reduced abundance of inflammation-related genes in the gut microbiota were potentially associated with a control group with long-term vegetarians. Thus, the composition and duration of the diet may have an impact on the balance of pro-/anti-inflammatory factors in the gut microbiota and immune system.

INTRODUCTION:Oxidative stress has been considered to play a primary role in the pathogenesis of stress-induced gastric damage. The aim of this study was to investigate the effects of melatonin, ascorbic acid andβ-carotene on stress-induced gastric mucosal damage.

MATERIAL AND METHODS:Fifty-six male Wistar albino rats were divided into control, stress, stress + standard diet, stress + saline, stress + melatonin, stress + ascorbic acid and stress +β-carotene groups. The rats from stress groups were exposed to starvation, immobilization and cold by immobilizing for 8 h at +4°C following 72-hour food restriction. Following stress application, melatonin, ascorbic acid and β-carotene were administered for 7 days. Specimens of gastric tissue were prepared for microscopic and biochemical examinations.

RESULTS:Mean histopathological damage scores and mean tissue malondialdehyde levels were significantly decreased but mean tissue glutathione levels and glutathione peroxidase and superoxide dismutase activities were increased in treatment groups vs. stress groups in general. Mean histopathological damage scores of the stress + Mel group was lower than those of stress + D, stress + S, stress +β-car (p<0.05) and stress + Asc groups (p<0.005). Additionally, mean tissue catalase activity of the stress + Mel group was higher than that of stress + S (p<0.005), stress + D (p<0.05) and stress +β-car groups (p<0.05).

CONCLUSIONS:Melatonin is more effective than ascorbic acid andβ-carotene in improvement of gastric damage induced by intensive stress. We suggest that as well as the direct antioxidant and free radical scavenging potency of melatonin, its indirect effect via the brain-gut axis might account for its greater beneficial action against stress-induced gastric damage.

BACKGROUND:Gynecological malignancies represent a major cause of death in women and are often treated with platinum-based regimens. Patients undergoing chemotherapy suffer from alterations in nutritional status which may worsen gastrointestinal (GI) toxicities, quality of life and affect the overall prognosis. Indeed, assuring a good nutritional status and limiting toxicities during treatment are still major goals for clinicians.

AIM:To assess the role of Mediterranean Diet (MD) in reducing GI toxicities in patients with gynecological cancers treated with platinum-based regimens.

METHODS:We conducted an observational study on 22 patients with gynecological tumors treated with a platinum-based chemotherapy at Candiolo Cancer Institute FPO/IRCCS between January 2018 and June 2018. The food and frequency (FFQ) and the Patient-Reported Outcomes Common Terminology Criteria For Adverse Events (PRO-CTCAE) questionnaires were administered at baseline and at every Day 1 of each cycle. To evaluate the differences in GI toxicities the study population was divided in two groups according to the currently validated Mediterranean Diet Serving Score (MDSS) at baseline.

RESULTS:Patients with high MDSS reported a trend toward lower GI toxicities according to PRO-CTCAE at each timepoint (first evaluation:= 0.7; second:= 0.52; third:= 0.01). In particular, difference in nausea frequency and gravity (<0.001), stomach pain frequency and gravity (= 0.01 and= 0.02), abdomen bloating frequency and gravity (= 0.02 and= 0.03), and interference with daily activities (= 0.02) were highly statistically significant at the end of treatment. More than 60% of patients changed their food habits during chemotherapy mainly because of GI toxicities. A higher reduction of food intake, both in terms of caloric (= 0.29) and of single nutrients emerged in the group experiencing higher toxicity.

CONCLUSION:Our results show that adherence to MD possibly reduces GI toxicity and prevents nutritional status impairment during chemotherapy treatment. Bigger studies are needed to confirm our results.