1.Progesterone regulates COX-2 and Caspase-3 expressions in hippocampal neurons in rats after traumatic brain injury by NF-?B signaling pathway
Jingshan MENG ; Daowen SI ; Zuofeng ZHANG ; Yuxin ZHANG ; Ziming ZHANG
Journal of Third Military Medical University 1984;0(02):-
Objective To investigate the effect of nuclear factor-?B(NF-?B) on the regulation of cyclooxygenase-2(COX-2) and Caspase-3 in hippocampal neurons after traumatic brain injury(TBI) in rats,and explore the neuroprotective effect and the possible mechanism of progesterone(PROG) in hippocampal neurons after TBI.Methods Forty-five male Spraque-Dawley rats were randomly divided into 3 groups: sham-operated group(n=15),TBI group(n=15) and PROG-treated group(n=15,intraperitoneal injection of PROG 16 mg/kg in 1 and 6 h after injury).The rat model of TBI was duplicated with the improved Feeney's method.The rats were sacrificed in 24 h after injury and their brain was resected.Nissl staining,immunohistochemical staining and Western blot assay for NF-?B,COX-2 and Caspase-3 was used to observe the changes of positive cell numbers and protein levels in the hippocampal neurons.Results The numbers of immunoreactive neurons to NF-?B(24.0?2.5),COX-2(35.9?2.7) and Caspase-3(25.1?2.7) were significantly increased in the hippocampus at 24 h after TBI when compared with the positive neuron numbers of NF-?B(1.9?0.9),COX-2(1.5?0.7) and Caspase-3(1.8?0.8) in sham group.After the treatment of PROG,the positive cell number of NF-?B(14.2?1.8),COX-2(16.6?2.7),Caspase-3(11.2?2.4) was reduced obviously as compared with the TBI group(P
2.Anatomical study of greater occipital nerve entrapment syndrome
Tingcai ZHANG ; Daowen SI ; Lihua LIU ; Yuxin ZHANG
Clinical Medicine of China 2008;24(7):655-656
ObjecUve To provide anatomical basis for diagnosis and therapeutic methods for treating grea-ter occipital nerve entrapment syndrome.Methods With 10 multiples microscope,the trace,distribution,compres-sion and relationship with occipital vessel of greater occipital nerve were observed and measured on 60 specimens of adult corpse.With a vernier caliper the distance of the easily compressed part of greater occipital nerve with external occipital protuberance,mastoidal and superior nuchal line were measured,and the superficial projeetion of the easily compressed part was marked.Results The course of the nerve could be divided into two parts:active part and inac-tive part.The former laid in the nuchal muscles,the latter ran and anchored to superficial fascia of the scalp,and easily compressed,accompanying with occipital vessel.This point lay in medial to occipital vessel and lateral to ex-ternal occipital protuberance(27.60±5.20)mm,and inferior to superior nuchal line(18.46±5.12) mm,and the superficial projection lay in median and superior 1/3 of the line from external occipital protuberance to mastoid apex. Conclusion Treating the greater occipital nerve compression syndrome by closed operation,the best position for needling lays in a bit inferior to point of median and superior 1/3 of the line from external occipital protuberance to mastoid apex.During the operation we should loose the main trunk compression of the greater occipital nerve as well as the branches compression on it.
3.Research on shape changes of tibiofibular syndesmosis following fibula resected from different positions
Tingcai ZHANG ; Daowen SI ; Yuxin ZHANG ; Shilong LI
Clinical Medicine of China 2009;25(3):275-276
Objective To investigate the different effects of different resection position of fibula on shape of tibiofibular syndesmosis,and explore the best position of cut fibula,providing reference for clinical surgeon to use fibula reasonably.Methods Ten adult male cadaverie specimens 172-176 cm long were used for 20 shank-ankle specimens.10 cm long fibula was cut proximally at the lower point 1/6,lower point 1/4,lower point 1/3,middle point 1/2 respectively,which was compared with the nornlal one to analyze the changes of shape of tibiofibular syndesmosis.Results Normally,the distance oftibiofibular syndesmosiswas(0.30±0.10)mm.Underthe condition of cut at the lower point 1/6,the distance of tibiofibular syndesmosis was enlarged[(0.54±0.20)mm](P<0.05).In contrast,under the condition of cut 10 cm long fibula proximally at the middle point 1/2.the distance of tibioffbu1ar syndesmosis hadlittle effect[(0.31±0.20)mm](P>0.05).Conclusion The best resection position of fibula is in the proximity of the fibula at the point 1/2.
4.Regulative role of progesterone in inflammatory reaction after traumatic brain injury in rats
Daowen SI ; Qingguo MA ; Dianyou HE ; Zhisheng KAN ; Jingshan MENG ; Yuxin ZHANG ; Ziming ZHANG
Chinese Journal of Trauma 2011;27(12):1140-1144
Objective To investigate the effect of progesterone on the expressions of inflammation-related factors of cortical cyclooxygenase-2 ( COX-2 ),prostaglandin E2 ( PGE2 ),inducible nitric oxide synthase (iNOS) and NF-κB in the cortex after traumatic brain injury (TBI) in rats so as to study the possible molecular mechanism of neuroprotective effect of progesterone on TBI.Methods Fortyfive male Spraque-Dawley rats were enrolled in the study and randomly divided into three groups,ie,sham operation group (n =15),TBI group (n =15) and progesterone treatment group (n =15).The rat model of TBI was duplicated with the improved Feeney' s method.The PROG treatment group was given i.p.injections of progesterone ( 16 mg/kg) at 1 and 6 hours after injury.The rats were sacrificed in three groups at 24 hours after injury and the specimens were removed.The changes of the positive cell numbers and protein level of COX-2,PGE2,iNOS and NF-κB in the cortex were examined by immunohistochemistry and Western blot.Results The positive cell numbers and protein levels of COX-2,PGE2,iNOS and NF-κB in the cortex of the TBI group were distinctly higher than those of the sham operation group (P<O.05).While the positive cell numbers and protein levels of COX-2,PGE2,iNOS and NF-κB in the cortex of the progesterone treatment group were distinctly lower than those of the TBI group ( P <O.05).Conclusions Progesterone may exert protective effect on TBI through inhibiting NF-κB activity,blocking the inflammation response course of NF - κB and iNOS and decreasing the expressions of COX-2 and PGE2.