Basic fibroblast growth factor promoting the healing of palatal perforation in rats

AIM: To study the influence of basic fibroblast growth factor(bFGF) on treating ed palatal perforation in rats. METHODS: bFGF was given to the early palatal perforation in rat. The granulation tissues in perforations were grossly and pathologically obserVed. RESULTS: The the of wound healing was significantly in- crease in the bFGF group (P<0.01 ). bFGF could obviously promote the proliferation of the granulation tissues and fibroblasts. The number of AgNORs granules in fibrablasts were 3.73 ±0.52 in the buy group and 2.11 ±0.31 in control group (P < 0.05). CONCLUSION: bFGF could promote the growth of granulation tissues and had a strong promotion on the wound healing in palatal perforation. It was helpful in repairing palatal perforation.     

Coriaria sinica Maxim extract promotes burn wound healing in rats

AIM：To investigate the effects of Coriaria sinica Maxim extract (CSME) on burn wound healing in rats. METHODS：Forty male SD rats were randomly divided into normal saline (NS) group, white petrolatum jelly (WPJ) group, silver sulfadiazine (SSD) group and CSME group. After the animals were anesthetized, the skin of their backs was burnt to induce deep Ⅱ degree burn wounds. These wounds were treated respectively for 21 d by covering dressings with NS, WPJ, SSD and CSME, respectively. On the 1st, 3rd, 7th, 14th and 21st days, after the clinical symptoms of the animals and conditions of the wounds such as the epithelization rate, crusting and hair growth were observed, the wound tissues were also taken for histological examination. The content of malondialdehyde (MDA), the activity of superoxide dismutase (SOD), and the expression of epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and collagen were detected. RESULTS：On the 21st day after burn, the new epithelial tissues in CSME group extraordinarily　developed and a great deal of hair also grew along the margin of the wounds. The epithelization rate of the wound tissues in CSME group was higher than that in other groups. There was rare new hair in the center of the wound area in SSD group, but intensive new hair was observed in CSME group. On the 14th day and 21st day after burn, multilayer of epithelial cells was entirely covered with the wound area in CSME group. Some of the healing signs, such as sufficient differentiation and a line up in order of collagen fibers, clear tissue structure, exceedingly active hyperplasia of sebaceous glands and hair follicles, and so on, were also observed in the wound area in CSME group. From the 1st day to 21st day after burn, the increase in protein expression of EGF and bFGF in the wound tissues was significantly higher than that in other groups in the early stage, which was quickly decreased and was obviously lower than other groups in the latter stage. The mRNA expression ratio of type I and III collagens in SSD group was significantly higher than that in other groups, while that in CSME group was significantly lower than that in other groups. CONCLUSION：CSME promotes burn wound healing without scarring. The effects of CSME are likely to associate with the expression reinforcement of EGF and bFGF at mRNA and protein levels in the early stage, and associate with the expression inhibition of them later. Moreover, CSME may also inhibit the mRNA expression of type I collagen and promote the synthesis of type III collagen in the wound tissues of burn.     

Antagonistic effect of angiotensin II type 1 receptor blocker candesartan on angiotensin II-induced proliferation of primary acute myeloid leukemia cells

AIM: To explore the antagonistic effect and mechanism of candesartan on angiotensin II (Ang II)-induced proliferation of primary acute myeloid leukemia (AML)cells. METHODS: MTT assay was used to observe the proliferation effect of Ang II on primary AML cells and normal bone marrow mononuclear cells, and the antagonistic effects of candesartan and PD123319 (an antagonist of AT2R) were also observed. Akt phosphorylation was detected by Western blotting when the cells were treated with candesartan and a PI3K inhibitor LY294002.RESULTS: Compared with the control cells, Ang II significantly increased the proliferation of AML cells in a dose-and time-dependent manner (P<0.05). Ang II did not stimulate the proliferation of normal bone marrow mononuclear cells. The proliferative effect of Ang II was effectively blocked by the AT1R blocker candesartan (P<0.05). PI3K inhibitor strongly repressed the Ang II-induced cell proliferation (P<0.05). Candesartan significantly reduced Akt phosphorylation promoted by Ang II on primary AML cells (P<0.05).CONCLUSION: Candesartan effectively inhibits Ang II-induced proliferation of primary AML cells by down-regulating PI3K/Akt signaling pathway, indicating a new possible treatment mechanism in some AML cells.     

Effect of AT2 receptor on the proliferation and the NOS expression in cultured adult rat VSMC

AIM: To observe the effect of angiotensinⅡ subtype 2 receptor (AT2 receptor) on the cultured rat aortic vascular smooth muscle cells. METHODS: The plasmid contained the cDNA of AT2 receptor was transfected into cultured rat vascular smooth muscle cells. The effects of AngⅡ, Ang Ⅱ＋losartan, Ang Ⅱ+PD123319 on the expression of PCNA, the NOS activity and the cell number were observed. RESULTS: The cell number and the expression of PCNA decreased after the cells were treated with losartan. When treated with PD123319, the cell number and the expression of PCNA increased, but the expression of NOS decreased. CONCLUSIONS: These data suggest that when being activated, AT2 receptor inhibits the proliferation of vascular smooth muscle cells and antagonizes the effect of AT1 receptor, such an effect may be related to the activation of NOS.     

Effects of aldosterone on expression of angiotensin Ⅱ receptors in cultured rat mesangial cells

AIM: To investigate the effect of aldosterone (ALD) on the mRNA expression of angiotensin Ⅱ (Ang II) type 1 (AT-1a R and AT-1bR) and 2 (AT-2R) receptors in cultured rat mesangial cells (RMCs) treated with high glucose. METHODS: Rat mesangial cells were cultured in high glucose medium containing different concentrations of ALD (10-8-10-6 mol/L). The antagonists of ALD and Ang II receptors including pironolactone (10-7 mol/L, aldosterone receptor antagonist, SPI), losartan (10-7 mol/L, Ang II type 1 receptor blocker, Los) or PD123319 (10-9 mol/L, Ang II type 2 receptor antagonist, PD) were added in the cell culture for 12 h. The control cells were only treated with high (30 mmol/L) or normal (5.6 mmol/L) glucose medium. The viability and proliferation of the RMCs were evaluated by MTT assay. The mRNA expression of AT-1aR, AT-1b R and AT-2R was detected by semi-quantitative RT- PCR. The expression of MCP-1 in cultured RMCs was detected by ELISA. RESULTS: The mRNA expression of AT-1aR, AT-1b R and AT-2R was increased significantly by treatment with ALD in a dose-dependent manner (1.62-1.77, 9.61-9.89 and 7.26-7.35 folds of high glucose control, respectively, P<0.01). SPI significantly reduced the mRNA expression of AT-1aR and AT-1b R (P<0.01) but not affected the mRNA expression of AT-2R. The ratio of AT-1aR/AT-1b R in cultured RMCs treated with high glucose decreased significantly after stimulated with ALD (P<0.01). However, the effect of ALD was inhibited by SPI (P<0.01). Aldosterone treatment induced a significant upregulation of MCP-1 expression in a dose-dependent manner, and previous treatment with spironolactone, losartan or PD123319 abolished this aldosterone-induced MCP-1 expression. CONCLUSION: The results suggest that aldosterone is involved in the inflammatory response by up-regulating the expression of AT-1aR, AT-1bR and AT-2R, changing the proportion of AT-1R subtype, and inducing MCP-1 overproduction in cultured RMCs treated with high glucose.     

Effect of acupuncture on expression of EGF and bFGF in brain tissues of rats with traumatic brain injury

AIM: To observe the effect of acupuncture on the expression of epidermal growth factor (EGF) and basic fibrolblast growth factor (bFGF) in the brain tissues of rats with traumatic brain injury. METHODS: Thirty SD rats were randomized into sham-operated group, model group and acupuncture group. The model of traumatic brain injury was established by free drop impact. Acupuncture was performed to the rats in acupuncture group once every day and 7 days altogether. Brain histotomy was conducted after the treatment. Immunohistochemical method was adopted to test the protein expression of EGF and bFGF. RESULTS: Compared to sham-operated group, the expression of EGF in the brain tissues of model group decreased (P<0.01), and the expression of bFGF increased (P<0.01). Compared to model group, the expression of EGF and bFGF in acupuncture group increased obviously (P<0.01). CONCLUSION: Acupuncture significantly increases the expression of EGF and bFGF, and improves the repair of injured brain tissues. This might be one of the mechanisms by which acupuncture can treat traumatic brain injury and improve the nervous function.     

番茄/番茄嫁接体发育过程中的过氧化物酶同工酶

分析番茄 /番茄嫁接体发育过程中的过氧化物酶同工酶 ,发现嫁接接合部酶谱和活性变化与创伤处理及对照不同。嫁接及创伤处理均可诱导同工酶产生 ,但接合部同工酶的产生往往早于创伤部位 ,有的酶带的消失情况也与创伤不同。嫁接及创伤处理前 6d ,酶活性逐渐增加 ,变化类似 ,均明显高于对照 ,随后接合部酶活性逐渐高于创伤处理 ,第 15天 ,酶活性下降且低于伤口。可见嫁接体发育过程中 ,过氧化物酶的重要作用不仅局限于伤口的愈合。对嫁接体发育和伤口愈合的关系及过氧化物酶的作用进行了讨论     

Effects of basic fibroblast growth factor on proliferation and collagen production in human umbilical cord mesenchymal stem cells

AIM：To observe the growth pattern and surface markers of human umbilical cord mesenchymal stem cells(hUCMSCs) and to explore the influence of basic fibroblast growth factor (bFGF) on the proliferation and collagen production in hUCMSCs cultured in vitro. METHODS：hUCMSCs were isolated by enzyme digestion method and adherent culture. The surface markers CD45, CD34, CD105, CD29 and HLA-DR of the cells were analyzed by flow cytometry. The osteogenic ability and adipogenic differentiation were confirmed with oil red O and alizarin red staining. The optimal concentration of bFGF to promote the proliferation of hUCMSCs was 20 μg/L. The cells in control group were cultured in the growth medium consisting of DMEM/F12 and 10% volume fraction of fetal bovine serum. The cells in experiment group were cultured under the same condition of control group but plus 20 μg/L bFGF. The proliferation of hUCMSCs was analyzed by MTT assay. The expression of type I and III collagens at mRNA and protein levels was determined by RT-PCR and Western blotting. RESULTS：The growth curves indicated that bFGF promoted the proliferation of hUCMSCs. The hUCMSCs expressed CD29, but did not express CD34, CD45 or HLA-DR in the presence or absence of bFGF unanimously. The cells were alizarin red staining-positive and oil red O staining-positive. Compared with control group, the expression of type I and III collagens significantly decreased at mRNA and protein levels in experiment group. CONCLUSION：bFGF promotes the proliferation of hUCMSCs and does not change the expression of the surface markers. bFGF inhibits the expression of type I and III collagens at mRNA and protein levels, indicating that bFGF enhances the healing of wound without inducing scar hyperplasia.     

Recent advances in anti-basic fibroblast growth factor antibody

Basic fibroblast growth factor (bFGF) has been used in wound healing, bone healing, vascular grafting, lens regeneration and limp regeneration. Anti-bFGF antibody is thought to be an major important reagent for bFGF research. This review summarizes the development of anti-bFGF antibody in recent years including preparation, screening, identification and application in order to provide reference to the studies of this field in our country.     

Imbalance between matrix metalloproteinases and tissue inhibitor of metalloproteinases during wound healing in diabetic rats

AIM: To investigate the imbalance between the expression of metalloproteinases (MMPs) and that of tissue inhibitors of metalloproteinase (TIMPs) during wound healing in diabetic rats. METHODS: Diabetic rats were induced with streptozotocin. All rats were maintained for 6 weeks. A full-thickness excisional wound was created on the back of each rat. Every group was randomly divided into 3 subgroups of 7 rats: 3 d group, 7 d group, 14 d group and animals were killed at 3rd, 7th and 14th day. Routine pathological examination, Masson′s trichrome staining and immunohistochemistry were made to calculate the score of epidermal and dermal regeneration, granulation tissue thickness, angiogenesis, matrix density, and infiltrated cells at different time points. RT-PCR and Western blotting were used to detect the expression of mRNA and protein of MMP-9 and TIMP-1 in the skin at those time points. RESULTS: Six weeks after streptozotocin treatment, Three days after injury, the wound healing rate of normal rats was faster than that of diabetic rats. From 3rd to 14th day, there were a lot of fibroblast and macrophage in normal skin, while few such cells were observed in diabetic skin. The other histological scores in normal skin were higher than those in diabetic rats at 7th and 14th day. Both MMP-9 and TIMP-1 had minimally detectable levels before wounding but exhibited rapid, significantly large increases within 3 d after wounding. Subsequently, they showed a rapid decline by 14 d. The relative values of expression of MMP-9 mRNA and protein in diabetic group were higher than those in normal group at different time points. However, the values of TIMP-1 mRNA and protein in diabetic group were significantly lower than those in control group. Significant difference was observed between two groups with the ratio of MMP-9/TIMP-1, higher in diabetic group than that in normal group. CONCLUSION: Abnormal reepithelialization, angiogenesis, inflammatory cell infiltration, collagen fibers generation, granulation tissue deposition, seem to be the basic histopathology that delays wound healing. The imbalance between MMPs and TIMPs in diabetic skin tissue before and after injury may be one of the important reasons of these alterations of histopathology.     

Angiotensin II regulates catalase expression and promotes fibroblast phenotype transformation through ERK1/2 pathway

AIM: To explore the effect of extracellular signal-regulated kinase 1/2 (ERK1/2) on the vascular adventitial remodeling in a hypertension rat model. METHODS: The rats were randomly divided into control group, mini-pump infusion of saline group and mini-pump infusion of angiotensin II (Ang II) group as the hypertension model. The systolic pressure and vascular morphology of the rats were examined. Adventitial fibroblasts were treated with Ang II, PD98059 (ERK1/2 inhibitor) and Ang II+PD98059. The catalase (CAT) expression in the cells was detected by Western blotting. RESULTS: Compared with control group and mini-pump infusion of saline group, the systolic pressure and carotid media thickness (stained by HE) in mini-pump infusion of Ang II group were significantly increased (P<0.01). Meanwhile, artery morphology in mini-pump infusion of Ang II group had obviously changed with a significant occurrence of pathological vascular remodeling. The result of Western blotting showed that the expression of CAT in the adventitial fibroblasts treated with Ang II+PD98059 was much higher than that in the cells treated with Ang II alone (P<0.05), indicating that down-regulation of CAT induced by Ang II was restored by ERK1/2 signaling pathway. CONCLUSION: Ang II down-regulates CAT through ERK1/2 pathway and promotes cell phenotype transformation, which lead to pathological vascular remodeling.     

Effects of dexamethasone on acute lung injury by inhibiting renin-angiotensin system in rats

AIM:To explore the relationship between renin-angiotensin system (RAS) and acute lung injury (ALI) in rats, and the effect of dexamethasone (DEX) on RAS was observed.METHODS: The rat model of ALI was induced by hemorrhagic shock and LPS administered intraperitoneally. The changes of MAP and the effects of DEX on MAP were observed. The mRNA expressions of ACE, AGT, AT1 and AT2 in lung tissue were assayed by RT-PCR. The changes of Ang I and Ang II in the serum and the effects of DEX on them were observed.RESULTS: The increasing of MAP was statistically obvious. MAP in hemorrhagic shock+LPS (HL) group recovered more slowly than that in HL+DEX(HLD) group. ACE, AGT, AT1 and AT2 mRNA expressions in HL group were increased, and higher than those in HLD group. The change of Ang II in serum in HL group was obviously higher than that in HLD group, while that of Ang I was not obvious.CONCLUSION:ALI activates RAS in rat lung, and promotes the production of Ang II then aggravates the injury of lung through increasing the expression of ACE and AGT. DEX decreases expression of Ang II.     

Expression of VEGF and bFGF in rat model of pressure ulcer

AIM:To study the effects of vascular endothelial growth factor(VEGF) and basic fibroblast growth factor(bFGF) on the molecular pathogenesis of pressure ulcer.METHODS:SD rats were randomly divided into control group and experiment group. The pressure ulcer model was established by magnetic disk circulating compression method. HE staining was used to observe the pathological changes of the skin in the rats. The expression of VEGF and bFGF in the tissues was detected by immunohistochemical method. RESULTS:The expression of VEGF and bFGF in the tissues of rat Ⅲ-degree pressure ulcer was lower than that in the surrounding tissues and normal skin(P<0.01). The changes of VEGF and bFGF were consistent(κ=0.58). CONCLUSION:The expression levels of VEGF and bFGF are decreased in the tissues of rat pressure ulcer, suggesting that they may be the potential key factors in the difficult healing of pressure ulcer.     

Effects of hydrogen sulfide on wound healing of skin ulcer in diabetic rats

AIM: To study the effect of hydrogen sulfide on wound healing of skin ulcer in diabetic rats.METHODS: Male SD rats were randomly divided into 3 groups, including non-diabetic control(NDC) group, untreated diabetic control(UDC) group, and treated diabetic administration(TDA) group. Diabetic rats were induced by intraperitoneal injection of streptozotocin(STZ). After 1 week, wound healing model was prepared by making a round incision(2.0 cm in diameter) on the dorsal skin in full thickness. The rats from TDA group received 2% sodium bisulfide ointment on the skin ulcer wound, and the animals from UDC and NDC groups received control cream. After 21 d of treatment with sodium bisulfide, blood samples were collected for biochemical analysis, including prothrombin time(PT), thrombin time(TT), and fibrinogen(FIB) in plasma, as well as the activity of superoxide dismutase(SOD) and the content of malondialdehyde(MDA) in the serum. White blood cells(WBC) and lymphocytes were also counted. Granulation tissues from the wound were processed for histological examination and Western blot analysis was used to detect heme oxygenase-1(HO-1) and tumor necrosis factor α(TNF-α) expression.RESULTS: Compared with UDC group, sodium bisulfide treatment accelerated wound healing of skin ulcer(P<0.01), and increased the activity of SOD in serum(P<0.01) in the diabetic rats. The declined number of WBC and lymphocytes, prolonged PT and TT, and decreased FIB levels in rats treated with sodium bisulfied were also confirmed. Pathological section showed that there were inflammatory cell infiltration, and irregular and loose fibril alignment in the granulation tissue of rats from the UDC group, but there were regular fibril alignment and increased angiogenesis in the granulation tissue of rats from the TDA group(P<0.05). Furthermore, sodium bisulfide treatment raised HO-1 protein expression, and decreased TNF-α protein expression in the diabetic rats.CONCLUSION: Hydrogen sulfide accelerates the wound healing of skin ulcer in the rats with diabetes. The beneficial effect of H₂S may be associated with formation of granulation, anti-inflammation, and antioxidation.     

Effects of angiotensinⅡ and angiotensin-(1-7) on expression of(pro) renin receptor in rat vascular smooth muscle cells

AIM: To observe the effects of angiotensinⅡ (AngⅡ) and angiotensin-(1-7) on the expression of (pro)renin receptor in rat vascular smooth muscle cells.METHODS: The cultured VMSCs were randomly divided into control group, AngⅡ group, Ang-(1-7) group, AngⅡ+losartan (an AT₁ receptor antagonist) group, AngⅡ+PD123319(an AT₂ receptor antagonist) group and CGP42112A (an AT₂ receptor agonist)group. The expression of (P)RR at protein and mRNA levels was detected by Western blotting and real-time PCR,respectively.RESULTS: Compared with control group, AngⅡ distinctly increased and Ang-(1-7) decreased the expression of (P)RR mRNA and protein in VMSCs in a dose-dependent manner (P<0.01). Compared with AngⅡ group, losartan did not inhibit the expression of (P)RR mRNA and protein in VMSCs induced by AngⅡ (P>0.05), but PD123319 did (P<0.01). CGP42112A also induced the expression of (P)RR protein and mRNA in VMSCs (P<0.01).CONCLUSION: AngⅡ induces the expression of (P)RR in VMSCs by AT₂. However, Ang-(1-7) inhibits the expression of (P)RR in VMSCs.     

Placental growth factor is involved in angiotensin II-induced cardiac fibroblast activation

AIM：To explore the role of placental growth factor (PLGF) in the process of angiotensin II (Ang II)-induced activation of cardiac fibroblasts (CFs). METHODS：Primary culture and identification of CFs from neonatal Sprague-Dawley rats were performed. The method of fluorescence immunocytochemistry was employed to observe the expression of alpha-smooth muscle actin (α-SMA). Real-time PCR and Western blotting were used to determine mRNA and protein levels. The cell proliferation was observed by WST-1 assay. RESULTS：Compared with control group, the PLGF expression at mRNA and protein levels in Ang II-treated CFs was significantly increased, whereas the mRNA expression of PLGF was decreased in the CFs treated with telmisartan and Ang II. Treatment with PLGF induced the proliferation of CFs and increased the protein expression of α-SMA. Treatment with PLGF for 60 min significantly increased the protein levels of p-ERK1/2 in the CFs. Compared with Ang II group, the proliferation of CFs was depressed and the protein expression of α-SMA was attenuated in Ang II+anti-PLGF group.The mRNA expression levels of type I and type III collagens were also down-regulated. CONCLUSION：PLGF might be involved in the process of Ang II-induced proliferation of CFs and fibrosis.     

Role of post-hemorrhagic shock mesenteric lymph drainage in restoring balance of ACE/ACE2 in kidney of mice

AIM: To study the role of post-hemorrhagic shock mesenteric lymph (PHSML) drainage on the balance of angiotensin-converting enzyme (ACE) and ACE2 in the kidney. METHODS: A hemorrhagic shock model was established and then fluid resuscitation was performed to the animals in shock and shock+drainage groups, and the PHMSL was drained in shock+drainage group after fluid resuscitation. After 6 h of resuscitation, the mRNA expression of ACE, ACE2, angiotensin Ⅱ (Ang Ⅱ) type 1 receptor (AT1R) and Mas-related G-protein-coupled receptor (MasR), and the levels of Ang Ⅱ and Ang (1-7) in the renal tissues were observed. RESULTS: Hemorrhagic shock increased the levels of ACE mRNA, AT1R mRNA and Ang Ⅱ, and decreased the levels of ACE2 mRNA, MasR mRNA and Ang(1-7) in the kidney. PHSML drainage abolished the effect of hemorrhagic shock on ACE2 and AT1R mRNA expression. Meanwhile, PHSML drainage reduced the hemorrhagic shock-induced increases in the ratios of ACE/ACE2, Ang Ⅱ/Ang(1-7) and AT1R/MasR. CONCLUSION: The PHSML drainage restores the balance of ACE/ACE2, which is beneficial to alleviate acute kidney injury following hemorrhagic shock in the mice.     

Effects of angiotensionⅡon metalloproteinases and matrix in hypertrophied myocardium from infarcted rats

AIM: To investigate the roles of angiotensionⅡ (AngⅡ) receptors (AT₁, AT₂) antagonists on matrix metalloproteinases (MMPs) and extracellular matrix (ECM) system in septal myocardium from infarcted rats.METHODS: The model of rat myocardium infarction (MI) was established by permanent ligation of the left coronary artery. The treatments of the AT₁ receptor antagonist valsartan (10 mg·kg^-1·d^-1) or AT₂ receptor antagonist PD123319 (30 mg·kg^-1·d^-1) were started 7 days prior to surgery. On day 14 after MI, protein levels of MMP-2, 3, 9, fibronectin (FN), tenascin-C (TN-C) in interventricular septum (IS) were determined. The distributions of FN and TN-C were also determined by immunofluorescence.RESULTS: Pathological changes of IS on day 14 after MI showed typical myocardial hypertrophy. Protein expressions of MMP-2, 3, 9 and TN-C of IS in banding group were higher than those in sham-operation group (P<0.01). The expressions of TIMP-1 and FN were lower than those in sham-operation group (P<0.01). Protein expressions of MMP-2, 3, 9 and TN-C in valsartan group were obviously lower than those in banding and PD123319 groups (P<0.01). TIMP-1 and FN protein expressions in valsartan group were higher than those in banding and PD123319 groups (P<0.01). No difference between banding and PD123319 groups was observed (P>0.05).CONCLUSION: AngⅡis involved in myocardium remodeling in infarcted rats, which is mediated via AT₁ receptor to degrade matrix by MMPs. The heart protection of AT₁ receptor antagonists may relate to inhibition of MMPs.     

Endogenous hydrogen sulfide results in increase of reactive oxygen species induced by angiotensin II in neurons

AIM：To determine the effect of endogenous hydrogen sulfide (H2S) on the production of reactive oxygen species (ROS) in medullary neurons induced by angiotensin II (Ang II). METHODS：Primary cultured rat medullary neurons were used in the study. Identification of medullary neurons and the co-expression of cystathionine β-synthetase (CBS) were detected by double-labeling immunofluorescence. Medullary neurons were treated with Ang II in the presence or absence of sodium butyrate (NaBu, a CBS agonist; 100 μmol/L, 250 μmol/L and 500 μmol/L). ROS production was measured by dihydroethidium staining. The activity of total superoxide dismutase (SOD) was detected by ELISA. The mRNA expression of CBS was determined by real-time PCR. RESULTS：The medullary neurons in the cultured cells were over 90%. Ang II (1 μmol/L) significantly increased ROS level in the medullary neurons. Ang II inhibited the activity of total SOD in the medullary neurons. CBS was expressed in the medullary neurons. Ang II decreased the mRNA expression of CBS. NaBu (250 μmol/L and 500 μmol/L) inhibited ROS production induced by Ang II with a dose-dependent manner, while NaBu alone had no influence on the ROS level in the medullary neurons. CONCLUSION：Ang II increases the level of ROS in medullary neurons partly by inhibiting the activity of total SOD and the mRNA expression of CBS. Endogenous H2S inhibits the ROS level increased by Ang II in the medullary neurons.