Changes in flavor substances during the processing of boneless cold-eating rabbit meat.

Cold-eating rabbit is a traditional Chinese delicacy made by the process of pickling and frying. To explore the relationship between the flavor of cold-eating rabbit and the production process, this study investigated the changes of nucleotides, free amino acids, fatty acids, and volatile flavor substances in diced, marinated for 10 min, marinated for 20 min, fried for 5 min, re-fried for 10 min, re-fried for 15 min, re-fried for 20 min, seasoned and fried, and in the finished product, and analyzed the changes of flavor substances in deboned rabbit at different processing stages. Results showed that the content of 5'-inosine monophosphate (IMP) increased significantly (p < .05), indicating that the degradation pathway mainly involved IMP. In total, 17 free amino acids were detected, the contents of which increased significantly (p < .05). In addition, 27 medium- and long-chain fatty acids were detected. The total concentration of free fatty acids decreased in the fresh rabbit meat-marinated 20 min stage (p < .05), then increased in the fried 5 min-fried 20 min stage (p < .05), and finally decreased in the fried with spices-finished stage (p < .05). Seventy-seven volatile flavor substances were detected, and the 15-minute frying stage was key in producing the volatile flavor substances.

Non-enzymatic browning of a composite puree of Choerospondias axillaris, snow pear, and apple: kinetic modeling and correlation analysis.

Choerospondias axillaris, snow pear, and apple composite fruit puree can be affected by non-enzymatic browning during storage decreasing the market value of the product. This study aimed to explore, using kinetic methods, the effects of non-enzymatic precursors (polyphenols and ascorbic acid) and intermediates (5-hydroxymethylfurfural) on fruit puree stored at 4 °C for 35 days. The results showed that ascorbic acid fitted the first-order reaction model, while the 5-hydroxymethylfurfural was consistent with the complex reaction model. Furthermore, the 5-hydroxymethylfurfural content was 1.53 ± 0.18 mg/L, (corresponding to an increase of 565%), and the ascorbic acid content was 0.88 ± 0.22 mg/100 g, (corresponding to a decrease of 98.5%). The results also demonstrated a change in the titratable acid, soluble solids, and pH of the fruit puree. Finally, the correlation results revealed a significant correlation between non-enzymatic browning and 5-hydroxymethylfurfural, titratable acid, and pH (p < 0.05). Overall, the results suggest that the Maillard reaction could be responsible for the non-enzymatic browning of fruit purees during storage.

[Study on mechanism of curcumol against liver fibrosis based on autophagy and apoptosis of hepatic stellate cells].

The present study clarified the molecular mechanism of curcumol against liver fibrosis based on its effects on the autopha-gy and apoptosis of hepatic stellate cells. The hepatic stellate cells were divided into a blank control group, a transforming growth factor-ß1(TGF-ß1)(10 ng·mL~(-1)) group, and low-(12.5 mg·L~(-1)), medium-(25 mg·L~(-1)), and high-dose(50 mg·L~(-1)) curcumol groups. The effect of curcumol on the viability of hepatic stellate cells induced by TGF-ß1 was detected by the MTT assay kit. The apo-ptosis in each group was determined by flow cytometry. Real-time fluorescence-based quantitative PCR(RT-PCR) was employed for the detection of mRNA expression of α-smooth muscle actin(α-SMA), type Ⅰ collagen(collagen Ⅰ), and type Ⅲ collagen(collagen Ⅲ). Western blot was used to detect the protein expression of p62, microtubule-associated protein 1 light chain 3(LC3), beclin1, B cell lymphoma 2(Bcl-2), and Bcl-2-associated X protein(Bax). Transmission electron microscopy(TEM) was used to observe cell morphology and autophagosome formation in each group. The autophagic flux was observed after cell infection with adenovirus under double fluorescence labeling. The cell viability assay revealed that compared with the TGF-ß1 group, the curcumol groups showed significantly decreased cell viability. The apoptosis assay showed that the apoptosis rates of the curcumol groups were significantly higher than that of the TGF-ß1 group. RT-PCR indicated that the mRNA expression of α-SMA, collagenⅠ, and collagen Ⅲ in the curcumol groups was significantly lower than that of the TGF-ß1 group. Western blot showed that the expression of p62, LC3, beclin1, Bcl-2, and Bax in the curcumol groups was significantly different from that in the TGF-ß1 group. As demonstrated by TEM, compared with the TGF-ß1 group, the curcumol groups showed significantly increased autophagosomes. The detection of autophagic flow by the adenovirus under double fluorescence labeling showed that autolysosomes in the curcumol groups were significantly increased compared with those in the TGF-ß1 group. Curcumol can induce the autophagy and apoptosis of hepatic stellate cells, which may be one of its anti-liver fibrosis mechanisms.

Maternal exposure to imazalil disrupts intestinal barrier and bile acids enterohepatic circulation tightly related IL-22 expression in F0, F1 and F2 generations of mice.

There is a growing body of evidence linking maternal exposure of environmental pollutants to intestinal and metabolic diseases that can be conserved across multiple generations. Here, female C57BL/6 mice were treated imazalil (IMZ) at dietary levels of 0, 0.025‰ and 0.25‰ during the gestation and lactation periods. The results demonstrated that IMZ treatment not only induced significant changes in the mucus secretion and ionic transport, but also disrupted the expression of antimicrobial peptides in the intestine of F0, F1 and F2 generations. In addition, IMZ exposure altered BAs metabolism and the affected the expression levels of critical genes involved in BAs synthesis, signaling, transportation and apical uptake. The immune cell-produced cytokines were displaying extraordinary changes after IMZ exposure. In particular, whether it was in F0, F1-20d, F1-7 w or F2-20d, the expression of IL-22 had the trend of markedly increasing upon IMZ exposure. Correlation analyses revealed that the expression of IL-22 was positively correlated with the change of BAs metabolites. Together, all these results indicated that IMZ exposure was perceived as a major stress by the intestinal epithelium that strongly affected the intestinal barrier function (including mucus, CFTR, AMPs, inflammation), largely in response to an alteration of BAs metabolism.

Imidacloprid disturbed the gut barrier function and interfered with bile acids metabolism in mice.

The toxicity of neonicotinoid insecticide imidacloprid (IMI) to mammals has recently received increasing attention. However, the effects of IMI on the gut barrier and liver function of male C57BL/6J mice are still unknown. The study showed that exposure to IMI could reduce relative liver weights, change hepatic tissue morphology and induce hepatic oxidative stress. The gut barrier function was greatly impaired by IMI exposure, which might increase the body's susceptibility to harmful substances in the gut. Meanwhile, the synthesis and metabolism of hepatic bile acids (BAs) was also affected by IMI exposure. The levels of serum and hepatic total bile acids (TBAs) decreased; in contrast, the fecal TBA levels increased after exposure to 30 mg/L IMI for 10 weeks. Sequencing of colonic contents revealed that the operational taxonomic units (OTUs) and α-diversity index increased and that the gram-negative bacteria overgrew, indicating that the balance of the gut microbiota was disrupted. The present study indicated that subchronic exposure to IMI interfered with the gut barrier function, interfering with BAs metabolism and causing gut microbiota imbalance in male C57BL/6J mice. Taken together, IMI residues appear to be potentially toxic to mammals and even humans.

Imidacloprid disrupts the endocrine system by interacting with androgen receptor in male mice.

In the current study, six-week-old male ICR mice were administered imidacloprid (IMI) at concentrations of 3, 10 and 30 mg/L for a duration of 10 weeks to investigate the toxicity of IMI on the endocrine system. We observed that testicular morphology was severely impaired and damaged, and the levels of serum testosterone (T) and the expression of androgen receptor (AR) decreased significantly. Molecular docking analysis suggested that IMI docks into the active site of AR successfully and that three key hydrogen bonds were formed with the active site residues Glu11, Gln41 and Lys138. The binding free energy value of the AR-IMI complex suggested a stable binding between IMI and AR. All these results indicated that IMI could interact with AR. In addition, major genes in the testis involved in the synthesis of cholesterol and T were generally inhibited, and the serum cholesterol sources were also reduced. Moreover, the aromatase in male mice was lacking after subchronic IMI exposure. The data acquired from the present study indicated that IMI could lead to endocrine disruption by interacting with AR and influence the expression of genes involved in the production of T in male mice.

Subchronic exposure of environmentally relevant concentrations of F-53B in mice resulted in gut barrier dysfunction and colonic inflammation in a sex-independent manner.

F-53B (6:2 chlorinated polyfluorinated ether sulfonate) is currently recognized as a safe alternative to long-chain PFASs in China. However, an increasing number of studies have recently authenticated its biotoxicological effects. In this study, for evaluating the gut toxicity of F-53B in mammals, both female and male mice were orally exposed to 0, 1, 3, or 10 µg/L F-53B for 10 weeks. Our results showed that F-53B significantly accumulated in the colon, ileum and serum when exposed to 10 µg/L F-53B for 10 weeks. F-53B exposure not only increased the transcriptional levels of ion transport-related genes but could also interact with the CFTR protein directly. Interestingly, subchronic F-53B exposure also increased the transcription of mucus secretion-related genes, but the protein level of Muc2 decreased after F-53B exposure, indicating that there was a compensatory phenomenon after mucus barrier injury. Furthermore, F-53B exposure also induced colonic inflammation associated with gut microbiota dysbiosis in the colon. Taken together, our results indicated that the potential gut toxicity of F-53B and almost all of the changed parameters were significantly affected in both female and male mice, suggesting that F-53B could disturb the gut barrier without sex dependence in mice.

Gut microbiota: An underestimated and unintended recipient for pesticide-induced toxicity.

Pesticide pollution residues have become increasingly common health hazards over the last several decades because of the wide use of pesticides. The gastrointestinal tract is the first physical and biological barrier to contaminated food and is therefore the first exposure site. Interestingly, a number of studies have shown that the gut microbiota plays a key role in the toxicity of pesticides and has a profound relationship with environmental animal and human health. For instance, intake of the pesticide of chlorpyrifos can promote obesity and insulin resistance through influencing gut and gut microbiota of mice. In this review, we discussed the possible effects of different kinds of widely used pesticides on the gut microbiota in different experimental models and analyzed their possible subsequent effects on the health of the host. More and more studies indicated that the gut microbiota of animals played a very important role in pesticides-induced toxicity, suggesting that gut micriobita was also the unintended recipient of pesticides. We hope that more attention can focus on the relationship between pesticides, gut microbiota and environmental health risk assessment in near future.

Plumbagin induces autophagy and apoptosis of SMMC-7721 cells in vitro and in vivo.

Plumbagin (PL), an active naphthoquinone compound, has been demonstrated to be a potential anticancer agent. However, the underlying anticancer mechanism is not fully understood. In this study, the human hepatocellular carcinoma (HCC) SMMC-7721 cell line was studied in an in vitro model. The cell proliferation was inhibited by PL in a dose- and time-dependent manner. Electron microscopy, acridine orange staining, and immunofluorescence were used to evaluate autophagosome formation and LC3 protein expression in PL-treated SMMC-7721 cells. Real-time polymerase chain reaction and Western blot showed that PL treatment suppressed the expression of apoptosis and autophagy factors (LC3, Beclin1, Atg7, and Atg5), which are associated with tumor apoptosis and autophagy in SMMC-7721 cells. In the study of in vitro tumor nude mouse models, PL can inhibit tumor growth. Cell apoptosis and autophagy of the transplanted tumors were evaluated by hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining, and Western blot. In addition, in the in vivo studies of HCC cells, we found that pretreatment with the autophagy inhibitor 3-methyladenine blocked the formation of apoptosis induced by PL. In contrast, administration of the apoptosis inhibitor Z-VAD did not affect PL-induced autophagy. Taken together, our findings strongly suggest that PL is a promising drug with significant antitumor activity in HCC.

[Pharmacological study on hemostasis, analgesic and anti inflammation effects of the alcohol extract of Hibiscus tiliaceus].

OBJECTIVE: To study the effects of hemostasis, analgesic and anti inflammation of the alcohol extract of Hibiscus tiliaceus and offer pharmacological and experimental basis for its safe and effective use in clinic. METHODS: The effects of hemostasist were observed with tail breaking method, capillary tube method and slide method; Hot board and body distortion induced by acetic acid methods were applied in mice analgesia experiment, the mice model of acute auricle swelling induced by dmi ethylbenzene and capillary permeability induced by acetic acid were applied to observe the anti inflammatory effects. RESULTS: The alcohol extract of Hibiscus tiliaceus could significantly reduce the bleeding time and the clotting time, delay the plant reaction time and reduce the writhing times of the mice, and it also had effect on inhibiting swelling of mice ear and the permeability of the capillary. CONCLUSION: These results suggest that the alcohol extract of Hibiscus tiliaceus has the effects of hemostasis, analgesic and anti inflammation.