This work highlights the relationship of crosslink density, entanglement points and various sulfide crosslinks with the thermogenesis properties of natural rubber (NR). The impact of cross‐link and entanglement on thermogenesis properties was evaluated by heat build‐up test, swelling behavior, statistical thermodynamic calculation, and classic viscoelastic theory. It was found that cross‐link and entanglement points have “pinning” effect to the rubber chain, thus remarkably restricting the motion of the rubber chain and reducing thermogenesis. Besides, the effects of various sulfide crosslinks and cross‐link length on thermogenesis were compared and discussed varying the sulfur vulcanization system. It was found that the semi‐effective vulcanization system using N‐cyclohexyl‐2‐benzothiazolesulfenamide (CZ) and 2‐Mercaptobenzothiazole (M) has the lowest thermogenesis (bottom temperature rise is 7.5°C, middle is 18.7°C), which on account of combined short crosslink length with high rigid rubber chain (crosslink network dominated by mono‐ and disulfides). As a result, the deformation degree of the rubber chain during curl up‐extension and the thermogenesis are further reduced. Finally, a combination of natural film coagulation and semi‐effective vulcanization system was used to prepare a low thermogenesis NR, in which bottom and middle temperature rise were only 5.0°C and 14.1°C, respectively.
AimsFew treatments are available in the subacute phase of traumatic brain injury (TBI) except rehabilitation training. We previously reported that transient CO2 inhalation applied within minutes after reperfusion has neuroprotective effects against cerebral ischemia/reperfusion injury. In this study, it was hypothesized that delayed CO2 postconditioning (DCPC) starting at the subacute phase may promote neurological recovery of TBI.MethodsUsing a cryogenic TBI (cTBI) model, mice received DCPC daily by inhaling 5%/10%/20% CO2 for various time‐courses (one/two/three cycles of 10‐min inhalation/10‐min break) at Days 3–7, 3–14 or 7–18 after cTBI. Beam walking and gait tests were used to assess the effect of DCPC. Lesion size, expression of GAP‐43 and synaptophysin, amoeboid microglia number and glia scar area were detected. Transcriptome and recombinant interferon regulatory factor 7 (Irf7) adeno‐associated virus were applied to investigate the molecular mechanisms.ResultsDCPC significantly promoted recovery of motor function in a concentration and time‐course dependent manner with a wide therapeutic time window of at least 7 days after cTBI. The beneficial effects of DCPC were blocked by intracerebroventricular injection of NaHCO3. DCPC also increased puncta density of GAP‐43 and synaptophysin, and reduced amoeboid microglia number and glial scar formation in the cortex surrounding the lesion. Transcriptome analysis showed many inflammation‐related genes and pathways were altered by DCPC, and Irf7 was a hub gene, while overexpression of IRF7 blocked the motor function improvement of DCPC.ConclusionsWe first showed that DCPC promoted functional recovery and brain tissue repair, which opens a new therapeutic time window of postconditioning for TBI. Inhibition of IRF7 is a key molecular mechanism for the beneficial effects of DCPC, and IRF7 may be a potential therapeutic target for rehabilitation after TBI.
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