Fig 1.
A: the principle of NAIs production in this study. B: three original data from an ultrasensitive chemiluminescence analyzer. C: statistical difference between saline and NAIs treated saline (Saline + Ni). Data were expressed as mean ± SEM (n = 6). * P < 0.05 between two groups comparision.
Fig 2.
The physiologic parameters including mean blood pressure (MAP) and respiratory rate in response to LPS or NAIs in four groups of rats.
A: the original data from four groups of rats. B: the statistical data of MAP in four groups of rats. C: the statistical data of respiratory rate in four groups of rats. Data were expressed as mean ± SEM (n = 9). * P < 0.05 vs. Saline groups.
Fig 3.
Effect of 60-min NAIs treatment on c-caspase 3 expression in LPS induced ALI for 210 min of four groups of rats.
A: original western blot of caspase 3. B: typical caspase 3 immunohistochemic graphs of four groups of rat lungs. C: Statistical data of caspase 3 western blot. D: Statistical data of pulmonary immunohistochemic caspase 3 stains. Data are expressed as mean ± SEM (n = 9). * P < 0.05 vs. Saline group. # P < 0.05 vs. LPS group.
Fig 4.
Effect of 60-min NAIs treatment on PARP expression in LPS induced ALI for 210 min of four groups of rats.
A: original western blot of PARP. B: typical PARP immunohistochemic graphs of four groups of rat lungs. C: Statistical data of PARP western blot. D: Statistical data of pulmonary immunohistochemic PARP stains. Data are expressed as mean ± SEM (n = 9). * P < 0.05 vs. Saline group. # P < 0.05 vs. LPS group.
Fig 5.
Effect of 60-min NAIs treatment on leukocyte infiltration, TUNEL expression, larvage neutrophils and larvage ROS in LPS induced ALI for 210 min of four groups of rats.
A: H&E stained lung sections of four groups of rats. B: statistical data of leukocyte infiltration of four groups of rat lungs. C: original graphs of TUNEL stains of four groups of rat lungs. D: Statistical data of pulmonary TUNEL stains of four groups of rats. E: Larvage neutrophils number and F: Larvage ROS amount in four groups of rats. Data are expressed as mean ± SEM (n = 9). * P < 0.05 vs. Saline group. # P < 0.05 vs. LPS group.
Fig 6.
Effect of 60-min NAIs treatment on Beclin-1 expression in LPS induced ALI for 210 min of four groups of rats.
A: original western blot of Beclin-1. B: typical Beclin-1 immunohistochemic graphs of four groups of rat lungs. C: Statistical data of Beclin-1 western blot. D: Statistical data of pulmonary immunohistochemic Beclin-1 stains. Data are expressed as mean ± SEM (n = 9). * P < 0.05 vs. Saline group. # P < 0.05 vs. LPS group.
Fig 7.
Effect of NAIs treatment on LC3-II expression in LPS induced ALI of four groups of rats.
A: original western blot of LC3-II. B: typical immunohistochemic graphs of four groups of rat lungs. C: Statistical data of LC3-II western blot. D: Statistical data of pulmonary immunohistochemic LC3-II stains. Data are expressed as mean ± SEM (n = 9). * P < 0.05 vs. Saline group. # P < 0.05 vs. LPS group.
Fig 8.
Effect of NAIs exposure on the wound healing rate of rat skin of four groups of rats.
A: Representative images of the wound surface in each group on days 0, 3, 7, 11, 14 and 21. B: The merged images of different color correlated different time frame of wound area in four groups of rats. At day 21, the pink colored area is markedly reduced in the Con + NI group and DM + NI group. C: Statistical data of % unclosed wound area over time of four groups of rats. Data are expressed as mean ± SEM (n = 6). * P < 0.05 vs. Con group. # P < 0.05 vs. DM group.
Fig 9.
Effect of NAIs exposure on H&E and Masson’s trichrome stain in rat skin in the wound healing of four groups of rats.
A: Representative images of H&E histology on wound sections at day 21 (black arrow: WBC; red arrow: RBC). B: Analyses of RBC accumulation of various treatment groups on day 21 (n = 3). C: Analyses of leukocyte infiltration of various treatment groups on day 21 (n = 3). D: Representative images of Masson’s trichrome stain (blue color) on wound sections at day 21. E: Analyses of dermal collagen expression by Masson’s stain of various treatment groups on day 21 (n = 3). Data are expressed as mean ± SEM (n = 3). * P < 0.05 vs. Con group. # P < 0.05 vs. DM group.
Fig 10.
A: Representative histological photographs of wounded skin neighbor tissue stained with Sirius red staining are shown (Scale bars: 20 μm). B: Quantitative histological evaluation of wounded skin neighbor skin collagen fiber expression at day 21 after wound creation. Data are expressed as mean ± SEM (n = 6). * P < 0.05 vs. Con group. # P < 0.05 vs. DM group.
Fig 11.
Effect of NAIs exposure on rat skin TGFβ1 and VEGFR-2 expression in the wound healing of four groups of rats.
A: Representative images of TGFβ1 and VEGFR-2 immunohistochemistry on wound sections at day 21. B: Analyses of TGFβ1 stain of various treatment groups on day 21 (n = 5). C: Analyses of VEGFR-2 stain of various treatment groups on day 21 (n = 5). Data are expressed as mean ± SEM (n = 5). * P < 0.05 vs. Con group. # P < 0.05 vs. DM group.