SlMDH3 Interacts with Autophagy Receptor Protein SlATI1 and Positively Regulates Tomato Heat Tolerance.

Autophagy, a highly conserved protein degradation system, plays an important role in protecting cells from adverse environmental conditions. ATG8-INTERACTING PROTEIN1 (ATI1) acts as an autophagy receptor, but its functional mechanisms in plants' heat stress tolerance remain unclear. In this study, using LC-MS/MS, we identified malate dehydrogenase (SlMDH3) as a SlATI1-interacting protein. Further studies showed that heat stress induced the expression of SlMDH3 and SlMDH3 co-localized with SlATI1 under both 22 °C and 42 °C heat treatment conditions. Moreover, silencing of SlMDH3 increased the sensitivity of tomato to heat stress, as evidenced by exacerbated degradation of chlorophyll; accumulation of MDA, H2O2, and dead cells; increased relative conductivity; and inhibition of stress-related gene expression. Conversely, overexpression of SlMDH3 improved tomato's heat tolerance, leading to opposite effects on physiological indicators and gene expression compared to SlMDH3 silencing. Taken together, our study suggests that SlMDH3 interacts with SlATI1 and positively regulates tomato heat tolerance.

Optimization of clofibrate with O-desmethyl anetholtrithione lead to a novel hypolipidemia compound with hepatoprotective effect.

Oxidative stress and inflammation were considered to be the major mechanisms in liver damage caused by clofibrate (CF). In order to obtain lipid-lowering drugs with less liver damage, the structure of clofibrate was optimized by O-desmethyl anetholtrithione and got the target compound clofibrate-O-desmethyl anetholtrithione (CF-ATT). CF-ATT significantly reduced the levels of plasma triglycerides (TG), total cholesterol (TC) in hyperlipidemia mice induced by Triton WR-1339. In addition, CF-ATT has a significantly protective effect on the liver compared with CF. The liver weight and liver coefficient were reduced. The hepatic function indexes were also decreased, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). Histopathological examination of the liver revealed that inflammatory cell infiltration, nuclear degeneration, cytoplasmic loosening and hepatocyte necrosis were ameliorated by administration with CF-ATT. The hepatoprotective mechanism showed that CF-ATT significantly up-regulated Nrf2 and HO-1 protein expression and down-regulated p-NF-κB P65 expression in the liver. CF-ATT has obviously antioxidant and anti-inflammatory activity. These findings suggested that CF-ATT has significant hypolipidemia activity and exact hepatoprotective effect possibly through the Nrf2/NF-κB-mediated signal pathway.

Curcumin inhibited the growth and invasion of human monocytic leukaemia SHI-1 cells in vivo by altering MAPK and MMP signalling.

Context: Curcumin, a polyphenolic compound extracted from the rhizome of the tropical plant Curcuma longa L. (Zingiberaceae), has been considered as a cancer chemopreventive drug by American National Cancer Institute.Objective: To examine the effect of curcumin on acute monocytic leukaemia SHI-1 cells in vivo.Materials and methods: The SHI-1 cells (1 × 106 cells in 0.1 mL PBS) were injected subcutaneously into the right flanks of the female SCID mice. Curcumin dissolved in olive oil (15 and 30 mg/kg) was administered (i.p.) to mice once a day for 15 days while the control group received olive oil injection. Tumour proliferation and apoptosis were examined by PCNA, TUNEL and cleaved caspase-3 staining. The expression of MAPK, NF-κB, MMP9, MMP2 and vimentin were confirmed by RT-PCR, immunohistochemistry or western blotting.Results: Administration of curcumin significantly inhibited tumour growth, as the tumour weight decreased from 0.67 g (control) to 0.47 g (15 mg/kg) and 0.35 g (30 mg/kg). Curcumin inhibited the expression of PCNA and increased the degree of TUNEL and cleaved caspase-3 staining in tumour tissue. The results of western blotting showed that curcumin treatment inhibited NF-κB and ERK signalling while activating p38 and JNK. Moreover, curcumin attenuated the mRNA transcription and protein expression of MMP2 and MMP9. Curcumin also suppressed the level of vimentin.Discussion and conclusions: Our study demonstrates that curcumin can inhibit the growth and invasion of human monocytic leukaemia in vivo, suggesting the possible use of curcumin for anti-metastasis in leukaemia and the value of determining its unique target.

Vesicle formation-related protein CaSec16 and its ankyrin protein partner CaANK2B jointly enhance salt tolerance in pepper.

Vesicle transport plays important roles in plant tolerance against abiotic stresses. However, the contribution of a vesicle formation related protein CaSec16 (COPII coat assembly protein Sec16-like) in pepper tolerance to salt stress remains unclear. In this study, we report that the expression of CaSec16 was upregulated by salt stress. Compared to the control, the salt tolerance of pepper with CaSec16-silenced was compromised, which was shown by the corresponding phenotypes and physiological indexes, such as the death of growing point, the aggravated leaf wilting, the higher increment of relative electric leakage (REL), the lower content of total chlorophyll, the higher accumulation of dead cells, H2O2, malonaldehyde (MDA), and proline (Pro), and the inhibited induction of marker genes for salt-tolerance and vesicle transport. In contrast, the salt tolerance of pepper was enhanced by the transient overexpression of CaSec16. In addition, heterogeneously induced CaSec16 protein did not enhance the salt tolerance of Escherichia coli, an organism lacking the vesicle transport system. By yeast two-hybrid method, an ankyrin protein, CaANK2B, was identified as the interacting protein of CaSec16. The expression of CaANK2B showed a downward trend during the process of salt stress. Compared with the control, pepper plants with transient-overexpression of CaANK2B displayed increased salt tolerance, whereas those with CaANK2B-silenced exhibited reduced salt tolerance. Taken together, both the vesicle formation related protein CaSec16 and its interaction partner CaANK2B can improve the pepper tolerance to salt stress.

Insights into Nb doping effects on the catalytic activity and SO2 tolerance of Mn-Cu/BCN catalyst for low-temperature NH3-SCR reaction.

Biochar-based supported denitration catalysts have shown tremendous potential in reducing NOx, while improving low-temperature NH3-SCR catalytic activity and SO2 tolerance still faces great challenges. In this work, Mn7-Cu3/BCN and Mn7-Cu3-Nbx/BCN catalysts were prepared by one-step wet impregnation. The enhanced effect of Nb doping on the catalytic performance and SO2 tolerance over the Mn7-Cu3/BCN catalyst was evaluated in the temperature range of 75-275 °C. The denitrification activity test showed that the introduction of an appropriate amount of Nb increased the catalytic activity and N2 selectivity of the catalyst. The NO conversion of Mn7-Cu3-Nb0.05/BCN with an optimum doping ratio of 0.05 wt% Nb was higher than 94% at 150-275 °C. The characterization results indicated that the introduction of Nb enhanced the interaction between the active components MnOx and CuOx, accelerated the electron transfer between elements, and thus improved the Mn4+/Mnn+ and Oα/(Oα+Oß+Oγ) proportions and redox performance. On the other hand, Nb modification increased the number of weakly acidic sites, which was beneficial for the adsorption and activation of the reducing agent NH3 under low-temperature conditions. Meanwhile, Nb could significantly improve the SO2 poisoning resistance of the Mn7-Cu3/BCN-S catalyst when SO2 was added to the reaction system. The NO conversion of Mn7-Cu3-Nb0.05/BCN remained above 75% after a 13.5 h reaction under 100 ppm SO2 and 5 vol% H2O at 225 °C. By combining experimental characterization results with DFT calculation results, we effectively confirmed that Mn7-Cu3-Nb0.05/BCN had good sulfur resistance, mainly because Nb could effectively inhibit the formation of manganese sulfate and promote the decomposition of ammonium bisulfate.

Sand and sand-GAC filtration technologies in removing PPCPs: A review.

Concerns have been raised about the risks that pharmaceuticals and personal care products (PPCPs) in aquatic environments posed to humans and the environment. In recent years, sand filtration has been used to potentially remove these emerging contaminants from water. However, there has been no review of the effectiveness of this technology to date. This paper presents a brief introduction of sand filtration types, reviews the current progress in PPCPs removal through sand filtration, and discusses the mechanisms behind this process and the combination of granular activated carbon (GAC) and sand as an enhanced sand-GAC filtration technology. Sand filtration achieves a reasonable but highly variable degree of PPCPs removal. Biodegradation and adsorption are the two main mechanisms of PPCPs removal, in particular the biodegradation since adsorption capacity of sand is relatively low. Other processes, such as bio-sorption and indirect adsorption, may also contribute to PPCPs removal. To compensate for the inadequate PPCPs removal through sand filtration, porous GAC has been combined with sand to develop sand-GAC filtration technologies. Serial, dual, and sandwich filters have been investigated, and significant removal enhancement has been observed, due to the strengthened adsorption capacity, suggesting the applicability of these variants. Future research focus, such as investigating the influence of different operational conditions on sand filter performance, obtaining a deeper understanding of the various removal mechanisms, and investigating of long-term performance of the filter used for PPCPs removal, are suggested.