Effect and mechanism of vitamin D on the development of colorectal cancer based on intestinal flora disorder.

BACKGROUND: To investigate the correlation between the level of circulating vitamin D and the development of colorectal cancer (CRC) and to clarify the effect and mechanism of vitamin D on the development of CRC. METHODS: Serum samples from 63 patients with CRC (CRC group) and 61 healthy volunteers (normal group) were collected. Azoxymethane + dextran sodium sulfate-induced CRC mouse model and dietary models with different doses of vitamin D were established to verify whether vitamin D supplementation could reverse the occurrence and development of CRC at the overall animal level. Intestinal barrier integrity and microbial defense response were evaluated by detection of intestinal flora and expression of related genes. RESULTS: In the clinical serum samples, compared with the normal group, the level of 25 (OH) D3 in the CRC group was relatively low (P < 0.01), which was consistent with the clinical situation in mice. Vitamin D deficiency aggravated the deterioration of enteritis and intestinal cancer in CRC mice, whereas the overall condition of CRC mice improved after vitamin D supplementation. Vitamin D has a significant regulatory effect on the homeostasis of the intestinal flora, particularly in the regulation of intestinal probiotics, Akkermansia muciniphila-mediated colon barrier integrity. CONCLUSIONS: Vitamin D deficiency is closely related to the high incidence of CRC, and vitamin D supplementation can inhibit the occurrence and development of CRC. Vitamin D plays a role in the reversal of CRC mainly through the regulation of intestinal flora, especially the regulation of A. muciniphila-mediated colon barrier integrity.

[Antiulcer effects and mechanism study of Veronicastrum axillare on ethanol induced gastric ulcer rats].

OBJECTIVE: To study the antiulcer effects and the mechanism of Veronicastrum axillare (Sieb. et Zucc) Yamazaki (VAY) on ethanol induced gastric ulcer rats. METHODS: Totally 48 healthy SD rats were randomly divided into 6 groups, i.e., the normal group, the model group, the ranitidine group, the high dose VAY group, the medium dose VAY group, and the low dose VAY group, 8 in each group. Rats in the normal group and the model group were administered with normal saline respectively. Rats in the ranitidine group were administered with 0.18% ranitidine suspension (at the daily dose of 0.027 g/kg) by gastrogavage. Those in the high dose VAY group, the medium dose VAY group, and the low dose VAY group were administered with VAY at the daily dose of 2.8 g/kg, 1.4 g/kg, and 0.7 g/kg by gastrogavage, once daily for 14 consecutive days. The gastric ulcer model was established using absolute ethanol after the last gastrogavage. The ulcer index and the ulcer inhibitory rate were compared. The concentrations of malonyldialdehyde (MDA), nitric oxide (NO), epidermal growth factor (EGF), and the activity of superoxide dismutase (SOD) in the serum and the homogenate of the gastric mucosa tissue were detected. RESULTS: Compared with the model group, the gastric ulcer index in the rest groups obviously decreased (P < 0.01). The ulcer index was dose-dependent with VAY (P < 0.01), with the highest gastric ulcer index shown in the high dose VAY group (P < 0.01). Compared with the normal group, the concentrations of MDA and NO significantly increased in the serum and the gastric mucosa tissue, the activity of SOD and the EGF content in the gastric mucosa tissue of rats in the model group significantly decreased (P < 0.01). Compared with the model group, the MDA concentrations in the serum and the gastric mucosa tissue decreased, the serum NO content increased, the NO content in the gastric mucosa tissue decreased, the serum SOD activity increased, the EGF content in the gastric mucosa tissue increased in the rest groups, all showing statistical difference (P < 0.05, P < 0.01). CONCLUSIONS: The water extract of VAY had significant effects on ethanol induced gastric ulcer. Its mechanisms might lie in reducing the generation of free radicals, promoting the oxygen free radical clearance, restraining lipid peroxidation, regulating and controlling the in vivo contents of NO and EGF.

The expression of classical swine fever virus structural protein E2 gene in tobacco chloroplasts for applying chloroplasts as bioreactors.

It has been reported that genes encoding antigens of bacterial and viral pathogens can be expressed in plants and are shown to induce protection antibodies. The structural protein E2 of classical swine fever virus (CSFV), which has been shown to carry critical epitopes, has been expressed in different systems. Here, we report the expression of CFSV E2 gene in tobacco chloroplasts. Mice immunized with leaf extracts elicited specific antibodies. This indicated that the expressed E2 proteins had a certain degree of immunogenicity. To our knowledge, this is the first report showing induction of protective antibody in response to classical swine fever virus (CSFV) by immunization with antigen protein E2 expressed in tobacco chloroplasts, which will open a new way to protection from CSFV by plant chloroplasts as bioreactors.

Stable expression of foot-and-mouth disease virus protein VP1 fused with cholera toxin B subunit in the potato (Solanum tuberosum).

The expression vector, pBI121CTBVP1, containing the fusion of the foot and mouth disease virus (FMDV) VP1 gene and the cholera toxin B subunit (CTB) gene was constructed by fused PCR and transferred into potato (Solanum tuberosum L.) by Agrobacterium-mediated transformation. Transformed plants were obtained by selecting on kanamycin-resistant medium strictly and regenerated. The transgenic plantlets were identified by PCR, Southern-blot and the production of fused protein was confirmed and quantified by Western-blot and ELISA assays. The results showed that the fused genes were expressed stablely under the control of specific-tuber patatin promoter. The expressed fused proteins have a certain degree of immunogenicity.