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With the increasing demand and quality requirement for the natural nutritious food in modern society, okra has attracted much attention because of its high nutritional value and remarkable functionality. However, the occurrence of postharvest diseases of fresh okra severely limited the application and the value of okra. Therefore, in this study, the dominant pathogens causing postharvest diseases such as soft rot were isolated from naturally decaying okra. It was identified as Mucor circinelloides by its morphological characteristics and standard internal transcribed spacer ribosomal DNA sequence. Furthermore, the biological characteristics of M. circinelloides were studied, and the inhibitory effect of thymol/KGM/LG (TKL) edible coating solution on M. circinelloides and its possible mechanism was discussed. In addition, TKL edible coating solution had a dose-dependent inhibitory effect on M. circinelloides, with a 50% inhibitory concentration (EC50) of 113.55 mg/L. The TKL edible coating solution at 960 mg/L of thymol completely inhibited mycelial growth and spore germination of M. circinelloides. The results showed that the best carbon source of M. circinelloides was maltose, the best nitrogen source was beef extract and potassium nitrate, the best pH was 6, the best temperature was 28°C, the best NaCl concentration was 0.5%, and the light was conducive to the growth of M. circinelloides. It was also observed by scanning electron microscope (SEM) that TKL was more likely to destroy the cell wall integrity of M. circinelloides, inhibit spore morphology and change mycelium structure. Meanwhile, the activity of chitinase (CHI), an enzyme related to cell wall synthesis of M. circinelloides, was significantly decreased after being treated by TKL with thymol at 100 mg/L (TKL100). The content of Malondialdehyde (MDA) in M. circinelloides decreased significantly from 12 h to 48 h, which may cause oxidative damage to the cell membrane. The activity polygalacturonase (PG), pectin methylgalacturonase (PMG), and cellulase (Cx) of M. circinelloides decreased significantly. Therefore, the results showed that TKL had a good bacteriostatic effect on okra soft rot pathogen, and the main bacteriostatic mechanism might be the damage of cell membrane, degradation of the cell wall, inhibition of metabolic activities, and reduction of metabolites, which is helpful to further understand the inhibitory effect of TKL on okra soft rot pathogen and its mechanism.

Inflammasomes play an important role in promoting heat stress (HS) induced liver injury. Dietary supplementation of camel whey protein (CWP) has been shown to alleviate HS-induced tissue damage. However, whether and how dietary CWP supplementation can reduce HS-induced liver injury remains unclear. Thus, we evaluated the ability of rats supplemented with CWP to resist HS-induced liver injury. To induce liver injury, Sprague-Dawley rats were exposed to HS. The mechanism of action was confirmed using an antagonist of high mobility group box 1 (HMGB1) and the NLR pyrin domain containing 3 (NLRP3) inhibitor before HS. Histological changes in the livers of the HS rats were visualised using haematoxylin and eosin staining. The protein expression of HMG1, receptor for advanced glycation end products (RAGE), NLRP3, Caspase-3, and Bcl-2 were detected using immunohistochemistry or western blotting. The content of IL-1β, the activation of Caspase-1, and the level of alanine transaminase (ALT) were determined using commercial kits. We confirmed that HS activated NLRP3 in the liver, as evidenced by enhanced Caspase-1 activity and increased IL-1β content. Inhibition of NLRP3 activation reversed abnormal expression and nuclear translocation of Caspase-3 and Bcl-2, and alleviated apoptosis, necrosis, and subsequent liver injury. HS-induced hepatocyte NLRP3 activation is dependent on elevated extracellular HMGB1 levels. Glycyrrhizic acid, an antagonist of HMGB1, which is also an anti-inflammatory agent, inhibited HS-induced NLRP3 activation. Interestingly, CWP also reversed HS-induced abnormal expression of HMGB1, RAGE, NLRP3, IL-1β, ALT, Bcl-2, and Caspase-3, inhibited Caspase-1 activity, and alleviated apoptosis and liver histological changes. More importantly, CWP combined with glycyrrhizic acid completely prevented HS-induced hepatocyte apoptosis and injury. These results indicate that CWP ameliorates HS-induced liver injury by inhibiting the HMGB1/RAGE/NLRP3 axis. Dietary supplementation with CWP may be an effective strategy to prevent serious complications from HS.

Gastrointestinal nematodes (GINs), such as Trichostrongylidae, are important pathogens in small ruminants, causing significant losses in these livestock species. Despite their veterinary importance, GINs have not been studied in certain regions of the world. Therefore, much of their epidemiology and economic impact on production remain unknown. In the present study, a systematic epidemiological survey based on the modified McMaster technique was conducted to investigate the type and infection of GINs in sheep and cattle. In 9622 fecal samples from 491 sampling sites in the four main banner districts of Ordos, the prevalence of GIN infection was found to be 38.84% and 4.48% in sheep and cattle, respectively. At the same time, the effects of four pasture types on the distribution of GINs were analyzed. This study also found severe resistance to ivermectin and albendazole in GINs and suspected anthelmintic resistance in nitroxynil, levamisole and closantel. We report the type and infection of GINs in Ordos, with the aim to help the prevention and control of GINs. Based on the results of the questionnaire survey and GIN resistance test, we found several reasons for the anthelmintic resistance of GINs, consequently providing new ideas for controlling the occurrence of anthelmintic resistance.