Microscopic investigations on the healing and softening of damaged salt by uniaxial deformation from CT, SEM and NMR: effect of fluids (brine and oil).

Nowadays, a salt cavern, used as underground energy storage (e.g. natural gas, crude oil, hydrogen), is becoming more and more popular in China due to its many advantages, such as low permeability (≤10-21 m2), good water-soluble mining and the damage-healing characteristic of salt rocks. It not only solves the problem of energy resource supply-demand imbalance in China, but also provides a better, more secure and cost-effective way to store energy compared to aboveground energy storage systems. As for salt cavern storage, permeability is our primary concern in engineering, which is mainly influenced by damage and healing. In this work, some damaged salt specimens were prepared by uniaxial compression tests (the loading rate was 0.033 mm s-1). Then those specimens were immersed in either a saturated brine solution or oil at 50 °C for a few days. Microscopic investigations were carried out by X-ray Computed Tomography (CT), Scanning Electron Microscope (SEM) and Nuclear Magnetic Resonance (NMR) to investigate the change of salt microstructures after healing. Possible micro-healing mechanisms were discussed. It was found that fluids played an important role in the healing process of damaged salt. Healing effectiveness of micro-pores and -cracks with the brine solution was higher than that with oil mainly because of crystal recrystallization. The surface of the grains was smooth and had no visible microcracks after healing in brine, while there were many pits and micro-tunnels with oil. Oil could hinder the healing process by impeding the diffusion effect and restraining grain recrystallization. Meanwhile, intragranular and intergranular water could also work as a lubricant resulting in softening which made salt rock more deformable. NMR results confirmed that damaged salt had a better recovery with brine, displaying lower porosity and lower permeability compared to that with oil. This work provides preliminary microscopic investigations on the healing of damaged salt in order to reveal the salt healing mechanism.

Molecular Mechanisms of Curcumin Renoprotection in Experimental Acute Renal Injury.

As a highly perfused organ, the kidney is especially sensitive to ischemia and reperfusion. Ischemia-reperfusion (IR)-induced acute kidney injury (AKI) has a high incidence during the perioperative period in the clinic and is an important link in ischemic acute renal failure (IARF). Therefore, IR-induced AKI has important clinical significance and it is necessary to explore to develop drugs to prevent and alleviate IR-induced AKI. Curcumin [diferuloylmethane, 1,7-bis(4-hydroxy-3-methoxiphenyl)-1,6-heptadiene-3,5-dione)] is a polyphenol compound derived from Curcuma longa (turmeric) and was shown to have a renoprotective effect on ischemia-reperfusion injury (IRI) in a previous study. However, the specific mechanisms underlying the protective role of curcumin in IR-induced AKI are not completely understood. APPL1 is a protein coding gene that has been shown to be involved in the crosstalk between the adiponectin-signaling and insulin-signaling pathways. In the study, to investigate the molecular mechanisms of curcumin effects in kidney ischemia/reperfusion model, we observed the effect of curcumin in experimental models of IR-induced AKI and we found that curcumin treatment significantly increased the expression of APPL1 and inhibited the activation of Akt after IR treatment in the kidney. Our in vitro results showed that apoptosis of renal tubular epithelial cells was exacerbated with hypoxia-reoxygenation (HR) treatment compared to sham control cells. Curcumin significantly decreased the rate of apoptosis in renal tubular epithelial cells with HR treatment. Moreover, knockdown of APPL1 activated Akt and subsequently aggravated apoptosis in HR-treated renal tubular epithelial cells. Conversely, inhibition of Akt directly reversed the effects of APPL1 knockdown. In summary, our study demonstrated that curcumin mediated upregulation of APPL1 protects against ischemia reperfusion induced AKI by inhibiting Akt phosphorylation.

Curcumin Attenuated Bupivacaine-Induced Neurotoxicity in SH-SY5Y Cells Via Activation of the Akt Signaling Pathway.

Bupivacaine is widely used for regional anesthesia, spinal anesthesia, and pain management. However, bupivacaine could cause neuronal injury. Curcumin, a low molecular weight polyphenol, has a variety of bioactivities and may exert neuroprotective effects against damage induced by some stimuli. In the present study, we tested whether curcumin could attenuate bupivacaine-induced neurotoxicity in SH-SY5Y cells. Cell injury was evaluated by examining cell viability, mitochondrial damage and apoptosis. We also investigated the levels of activation of the Akt signaling pathway and the effect of Akt inhibition by triciribine on cell injury following bupivacaine and curcumin treatment. Our findings showed that the bupivacaine treatment could induce neurotoxicity. Pretreatment of the SH-SY5Y cells with curcumin significantly attenuated bupivacaine-induced neurotoxicity. Interestingly, the curcumin treatment increased the levels of Akt phosphorylation. More significantly, the pharmacological inhibition of Akt abolished the cytoprotective effect of curcumin against bupivacaine-induced cell injury. Our data suggest that pretreating SH-SY5Y cells with curcumin provides a protective effect on bupivacaine-induced neuronal injury via activation of the Akt signaling pathway.