A separate-dural-incision method of extradural dumbbell spinal schwannoma resection: cumulative experience at a single center.

OBJECTIVE: To present our experience in the surgical management of completely extradural dumbbell spinal schwannomas with a new surgical strategy. METHOD: This study is a case series of patients treated at the Neurosurgery Department of the First Affiliated Hospital of USTC, between January 2018 and June 2021. RESULTS: 24 patients met the inclusion criteria, with cervical and lumbar spines being the most frequent locations. All patients underwent surgical treatment. Total gross resection was accomplished in all patients. Two cases had numbness and no case exhibited motor deficit. There was no postoperative CSF leakage or wound infection. CONCLUSION: Based on a limited number of observations, we conclude that our technique was feasible and effective for the treatment of extradural dumbbell spinal schwannomas. CLINICAL TRIAL: http://www.chictr.org.cn/ , No. ChiCTR2400086171.

The Upregulation of Molecules Related to Tumor Immune Escape in Human Pituitary Adenomas.

Human pituitary adenomas are one of the most common intracranial neoplasms. Although most of these tumors are benign and can be treated medically or by transsphenoidal surgery, a subset of these tumors are fast-growing, aggressive, recur, and remain a therapeutic dilemma. Because antibodies against immune checkpoint receptors PD-1 and CLTA-4 are now routinely used for cancer treatment, we quantified the expression of mRNA coding for PD-1, CLTA-4, and their ligands, PD-L1, PD-L2, CD80, and CD86 in human pituitary adenomas and normal pituitary glands, with the ultimate goal of exploiting immune checkpoint therapy in aggressive pituitary adenomas. Aggressive pituitary adenomas demonstrated an increased expression of PD-L2, CD80, and CD86 in compared to that of normal human pituitary glands. Furthermore, aggressive pituitary tumors demonstrated significantly higher levels of CD80 and CD86 compared to non-aggressive tumors. Our results establish a rationale for studying a potential role for immune checkpoint inhibition therapy in the treatment of pituitary adenomas.

Protocatechuic Acid Suppresses Microglia Activation and Facilitates M1 to M2 Phenotype Switching in Intracerebral Hemorrhage Mice.

OBJECTIVES: Microglia activation, a key process in secondary injury following intracerebral hemorrhage (ICH), is divided to M1 and M2 phenotype. Protocatechuic acid (PCA) is a phenolic acid been proved neuroprotection in ICH without understanding of details. Thus, this study aimed to observe the influence of PCA on microglia activation and explore underlying mechanisms. MATERIALS AND METHODS: To assess PCA affected microglia activation in vivo, an experimental ICH mice model was established and then treated with PCA intraperitoneal injection. Immunofluorescence staining was performed in brain slices at day 3 post ICH. BV2 cells were stimulated with hemin for activation, then M1 and M2 biomarkers were analyzed using Western Blot and qPCR. At last, we detected the expression of mTOR and its downstream molecules to discuss possible mechanisms. RESULTS: At day 3 post ICH, less activated microglia gathering around hematoma after PCA treatment. Furtherly, in hemin treated BV2 cells, PCA downregulated M1 and promoted M2 biomarkers expression in both mRNA and protein level. PCA inhibited the phosphorylation of mTOR, S6K1 and 4E-BP1, while the inhibition was disappeared after supplemented with mTOR activator. CONCLUSIONS: PCA impacted microglia activation by suppressing the mTOR signaling pathway, thereby improving M1/M2 switch and attenuated neuroinflammation.

Protocatechuic acid attenuates brain edema and blood-brain barrier disruption after intracerebral hemorrhage in mice by promoting Nrf2/HO-1 pathway.

The brain edema following intracerebral hemorrhage (ICH) plays a key role in the recovery process. Protocatechuic acid (PCA) has been proved possessing neuroprotection in ICH. Here we tried to explore its value in brain edema after ICH and reveal underlying mechanisms. ICH model was created in C57 mice using collagenase IV. PCA was injected intraperitoneally at 30 mg/kg every 24 h in PCA group. On day 3 after ICH, the water content of hemorrhagic ipsilateral hemisphere in PCA group was significantly reduced compared with vehicle group. AQP4, the main water channel, was remarkably decreased in PCA group. Additionally, ZO-1 and occludin expression were increased in PCA group. The bEnd.3 cells were cultured to understand the effect of PCA on the blood-brain barrier (BBB) integrity. Compare to hemin treated group, plus PCA enhanced the expression of HO-1 and Nrf2 nuclear translocation. Furtherly, the overexpression of HO-1, ZO-1, occludin, in the PCA treatment group was inhibited after knockdown of Nrf2. Taken together, our results proved PCA alleviated brain edema and BBB disruption in ICH by promoting the Nrf2/HO-1 signaling pathway.

Extracellular vesicle-carried microRNA-27b derived from mesenchymal stem cells accelerates cutaneous wound healing via E3 ubiquitin ligase ITCH.

Mesenchymal stem cells (MSCs) have been highlighted as promising candidate cells in relation to cutaneous wound healing. The current study aimed to investigate whether MSC-derived extracellular vesicles (EVs) could transfer microRNA-27b (miR-27b) to influence cutaneous wound healing. The miR-27b expression was examined in the established cutaneous wound mouse model, and its correlation with the wound healing rate was evaluated by Pearson's correlation analysis. The identified human umbilical cord MSC-derived EVs were co-cultured with human immortal keratinocyte line HaCaT and human skin fibroblasts (HSFs). The mice with cutaneous wound received injections of MSC-derived EVs. The effects of EVs or miR-27b loaded on wound healing and cellular functions were analysed via gain- and loss-of-function approaches in the co-culture system. Dual-luciferase reporter gene assay was employed to verify the relationship between miR-27b and Itchy E3 ubiquitin protein ligase (ITCH). Rescue experiments were conducted to investigate the underlying mechanisms associated with the ITCH/JUNB/inositol-requiring enzyme 1α (IRE1α) axis. miR-27b was down-regulated in the mouse model, with its expression found to be positively correlated with the wound healing rate. Abundant miR-27b was detected in the MSC-derived EVs, while EV-transferred miR-27b improved cutaneous wound healing in mice and improved proliferation and migration of HaCaT cells and HSFs in vitro. As a target of miR-27b, ITCH was found to repress cell proliferation and migration. ITCH enhanced the JUNB ubiquitination and degradation, ultimately inhibiting JUNB and IRE1α expressions and restraining wound healing. Collectively, MSC-derived EVs transferring miR-27b can promote cutaneous wound healing via ITCH/JUNB/IRE1α signalling, providing insight with clinical implications.

BM-MSC Transplantation Alleviates Intracerebral Hemorrhage-Induced Brain Injury, Promotes Astrocytes Vimentin Expression, and Enhances Astrocytes Antioxidation via the Cx43/Nrf2/HO-1 Axis.

Intracerebral hemorrhage (ICH) is a particularly severe form of stroke, and reactive astrogliosis is a common response following injury to the central nervous system (CNS). Mesenchymal stem cells (MSCs) are reported to promote neurogenesis and alleviate the late side effects in injured brain regions. Gap junctions (Gjs) are abundant in the brain, where the richest connexin (Cx) is Cx43, most prominently expressed in astrocytes. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an essential transcription factor regulating antioxidant reactions. Here, we aimed to explore whether bone marrow MSCs (BM-MSCs) could alleviate brain injury and protect astrocytes from apoptosis, by regulating Cx43 and Nrf2. We validated the effect of BM-MSC transplantation in an ICH model in vivo and in vitro and detected changes using immunofluorescence, as well as protein and mRNA expression of glial fibrillary acidic protein (GFAP), vimentin (VIM), Cx43, Nrf2, and heme oxygenase-1 (HO-1). Our results showed that BM-MSC transplantation attenuated brain injury after ICH and upregulated VIM expression in vivo and in vitro. Additionally, Cx43 upregulation and Nrf2 nuclear translocation were observed in astrocytes cocultured with BM-MSC. Knockdown of Cx43 by siRNA restrained Nrf2 nuclear translocation. Cx43 and Nrf2 had a connection as determined by immunofluorescence and coimmunoprecipitation. We demonstrated that astrocytes undergo astroglial-mesenchymal phenotype switching and have anti-apoptotic abilities after BM-MSC transplantation, where Cx43 upregulation triggers Nrf2 nuclear translocation and promotes its phase II enzyme expression. The Cx43/Nrf2 interaction of astrocytes after BM-MSC transplantation may provide an important therapeutic target in the management of ICH.

Bone marrow mesenchymal stem cells transplantation alleviates brain injury after intracerebral hemorrhage in mice through the Hippo signaling pathway.

Intracerebral hemorrhage (ICH) is a common acute nervous system disease with high mortality and severe disability. Mesenchymal stem cells (MSCs) have been reported to promote neurogenesis and to alleviate side effects in areas of brain injury areas. The Hippo pathway regulates diverse cellular processes, including cell survival, proliferation, differentiation, and organ size. Here, we found that transplantation of bone marrow MSCs (BM-MSCs) into the brains of mice could alleviate ICH-mediated injury and protect astrocytes from apoptosis by regulating mammalian sterile 20-like kinase (MST)1 and Yes-associated protein (YAP). Knocking down of MST1 by si-RNA triggered YAP nuclear translocation. We further demonstrated that astrocytes undergo astroglial-mesenchymal phenotype switching and become capable of proliferating after BM-MSC transplantation via the Hippo signaling pathway. Together, our identification of the Hippo pathway in mediating the beneficial effects of BM-MSCs may provide a novel therapeutic target in the treatment and management of ICH.

Melatonin Prevents Mice Cortical Astrocytes From Hemin-Induced Toxicity Through Activating PKCα/Nrf2/HO-1 Signaling in vitro.

Secondary injuries mediated by oxidative stress lead to deterioration of neurological functions after intracerebral hemorrhage (ICH). Cortical astrocytes are among the most important cells in the central nervous system (CNS), and play key roles in maintaining redox homeostasis by providing oxidative stress defense. Hemin is a product of hemoglobin degradation, which has strong toxicity and can induce reactive oxygen species (ROS). Melatonin (Mel) and its metabolites are well tolerated without toxicity, prevent tissue damage as well as effectively assist in scavenging free radicals. We evaluated the hemin neurotoxicity to astrocytes and the resistance of Mel-treated astrocytes to hemin neurotoxicity. And we found Mel induced PKCα phosphorylation (p-PKC), nuclear translocation of Nrf2 in astrocytes, and upregulation of HO-1, which contributed to the reduction of ROS accumulation and cell apoptosis. Nrf2 and HO1 protein expression upregulated by Mel were decreased after administration of PKC inhibitor, Ro 31-8220 (Ro 31). Luzindole (Luz), a melatonin receptor inhibitor, suppressed p-PKCα, HO-1, and Nrf2 expression upregulated by Mel and increased cell apoptosis rate. The upregulation of HO-1 induced by Mel was depressed by knocking down Nrf2 expression by siRNA, which also decreased the resistance of astrocytes to toxicity of hemin. Mel activates astrocytes through PKCα/Nrf2/HO-1 signaling pathway to acquire resistance to toxicity of hemin and resist from oxidative stress and apoptosis. The positive effect of Mel on PKCα/Nrf2/HO-1 signaling pathway may become a new target for neuroprotection after intracerebral hemorrhage.

Protocatechuic acid exerts protective effects via suppression of the P38/JNK- NF-κB signalling pathway in an experimental mouse model of intracerebral haemorrhage.

Protocatechuic acid (PCA) has been well studied for its neuroprotection value in several diseases, but the effect in intracerebral haemorrhage (ICH) has not been reported. Here we verified the protection of PCA in ICH, and investigated the relative mechanisms. ICH model mice were established by injection of collagenase IV. The mice were treated with PCA once per day for 3 days, starting immediately after operation. The modified neurological severity score (mNSS) of mice at 1st, 3rd and 7th day after operation were recorded. And some of mice were euthanized at 3rd day to compare brain water content, pro-inflammatory cytokines expression, and cell apoptosis in perihematomal tissue. Additionally, SH-SY5Y cells were treated hemin to mimic secondary injury of ICH. Cells were incubated with PCA for treatment. The cell viability, ROS, apoptosis rate and protein expression of apoptosis-relative protein and MAPKs and NF-κB were detected and analysed. The results revealed PCA alleviated the cerebral oedema at 3rd post ICH, and significantly improved neurological functions. PCA also attenuated the protein and gene expression of TNF-а, IL-1ß and IL-6 vivo. PCA dose-dependently decreased the generation of ROS and apoptosis rate. Furthermore, PCA treatment dose-dependently decreased the expression of bax, cleaved caspase-3, increased bcl-2 expression; PCA downregulated P38/JNK-NF-κB pathway. In conclusion, PCA effectively improves prognosis of ICH mice by inhibiting oxidative stress, inflammation and apoptosis. The mechanism possibly results of downregulating of P38/JNK-NF-κB pathway, and PCA can be a potential therapeutic agent for ICH.

Dexmedetomidine Promotes SH-SY5Y Cell Resistance Against Impairment of Iron Overload by Inhibiting NF-κB Pathways.

Iron overload is a common pathophysiological state underlying many diseases that has a detrimental influence on cells. The protective effects of Dexmedetomidine (Dex), a high selective alpha-2-adrenoceptor agonist, have been revealed through many experimental models, whereas no study reports its effects on an iron overload model. To elucidate these effects, we used FeCl2 with or without Dex to treat SH-SY5Y cells for 24 h and then detected indicators of oxidative stress, inflammation and apoptosis and investigated possible mechanisms further. After treatment with FeCl2 for 24 h, cell viability decreased in a dose dependent manner, and Dex promoted cell survival in FeCl2 incubation, also in a dose-dependent manner. Compared with the FeCl2 group, 20 µM Dex significantly attenuated ROS accumulation, reduced pro-inflammatory cytokine expression, and inhibited apoptosis. Furthermore, 20 µM concentration of Dex remarkably downregulated the expression of pro-apoptotic protein and activation of caspase 3 while increasing anti-apoptotic protein expression. Additionally, Dex also effectively suppressed the expression of NF-κB and its activation. In conclusion, Dex exerted anti-oxidative stress, anti-inflammation, and anti-apoptosis effects on FeCl2-treated SH-SY5Y cells, possibly by inhibiting NF-κB signaling pathway.

A connexin43/YAP axis regulates astroglial-mesenchymal transition in hemoglobin induced astrocyte activation.

Reactive astrogliosis is a common response to insults to the central nervous system, but the mechanism remains unknown. In this study, we found the temporal and spatial differential expression of glial fibrillary acidic protein (GFAP) and Vimentin in the intracerebral hemorrhage (ICH) mouse brain, indicating that the de-differentiation and astroglial-mesenchymal transition (AMT) of astrocytes might be an early event in reactive astrogliosis. Further we verified the AMT finding in purified astrocyte cultures exposed to hemoglobin (Hb). Additionally, Connexin 43 (Cx43) downregulation and YAP nuclear translocation were observed in Hb-activated astrocytes. Knocking down Cx43 by siRNA triggered YAP nuclear translocation. Cx43 and YAP were physically associated as determined by immunofluorescence and co-immunoprecipitation. We propose that astrocytes undergo AMT during Hb-induced activation where Cx43 downregulation facilitates YAP nuclear translocation is a novel mechanism involved in this process. Cx43-YAP interaction may represent a potential therapeutic target for modulating astrocyte activation.

Polymorphisms in the interleukin-1ß (IL-1B) and interleukin-1α (IL-1A) genes on risk of febrile seizures: a meta-analysis.

The aim of the current study was to clarify the role of four common genetic polymorphisms in the interleukin-1ß (IL-1B) and interleukin-1α (IL-1A) genes on risk of febrile seizures (FS) by means of meta-analyses. We searched for studies published until February 2018 using ISI Web of Science, Pubmed, Wanfang, and Chinese National Knowledge Infrastructure databases. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using MetaAnalyst version Beta 3.13. Seventeen case-control studies were included for meta-analysis. For the IL-1B rs16944 polymorphism, the summary analysis of studies conducted among Caucasian populations showed a significant association in the CT+TT versus CC contrast (OR 1.434, 95% CI 1.153-1.785), while the pooled analysis for Asian populations yielded a significant estimate in the TT versus CC+CT comparison (OR 1.393, 95% CI 1.051-1.846). No association was observed between the IL-1B rs1143627, IL-1B rs1143634, and IL-1A rs1800587 polymorphisms and FS risk. Sensitivity analyses excluding studies showing deviation from Hardy-Weinberg equilibrium did not alter conclusions. The findings of our meta-analysis suggest that the IL-1B rs16944 polymorphism may be an important genetic determinant for FS in Caucasian and Asian populations.

Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095.

The long non-coding RNA SNHG7 (small nucleolar RNA host gene 7) has been reported to be involved in various cancers as a potential oncogene. However, the functions and molecular mechanisms of SNHG7 in glioblastoma (GBM) are largely unknown. In the present study, we showed that the expression of SNHG7 was significantly upregulated in GBM tissues and cell lines compared with non-cancerous brain tissues. Furthermore, we found that SNHG7 knockdown remarkably suppressed the proliferation, migration and invasion of A172 and U87 cells while inducing their apoptosis. Subsequently, we showed that SNHG7 knockdown significantly inhibited tumor growth and metastasis in vivo by using xenograft experiments in nude mice. In terms of mechanism, we found that SNHG7 directly inhibited miR-5095, which targeted the 3' UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/ß-catenin signaling pathway in GBM. Using rescue experiments, we demonstrated that SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095 and concomitant activation of Wnt/ß-catenin signaling pathway. Taken together, the SNHG7/miR-5095 axis might be a potential target for the development of effective GBM therapy.

Hemoglobin pretreatment endows rat cortical astrocytes resistance to hemin-induced toxicity via Nrf2/HO-1 pathway.

Oxidative stress mediated secondary injury contributes to neurological deterioration after intracerebral hemorrhage (ICH). Astrocytes, the most dominant cells in the central nervous system (CNS), play key roles in maintaining redox homeostasis by providing oxidative stress defense. Hemoglobin (Hb), the primary component released by hemolysis, is an effective activator of astrocytes. Hemin, the product of Hb degradation, is highly toxic due to the induction of reactive oxygen species (ROS). We speculate that Hb-activated astrocytes are resistant to hemin-induced toxicity. To verify our speculation, Hb-pretreated astrocytes were exposed to hemin, intracellular ROS accumulation and cell apoptosis were evaluated. Heme oxygenase 1 (HO-1) and nuclear transcription factor-erythroid 2 related factor (Nrf2) expression were observed to explore the potential mechanism. The results demonstrated that Hb induced upregulation and nuclear translocation of Nrf2 in astrocytes, resulted in HO-1 upregulation, which contributed to reduced ROS accumulation and apoptosis rate. Knocking down Nrf2 expression by siRNA suppressed Hb-induced upregulation of HO-1 expression and increased the susceptibility of Hb-pretreated astrocytes to hemin-induced toxicity. Taken together, Hb-activated astrocytes acquired resistance to hemin-induced toxicity via Nrf2/HO-1 pathway. This phenomenon can be considered as the adaptive self-defense in the pathological process of ICH. Hb pre-warned astrocytes and enhanced their capability of handling the coming hemin "flood". Nrf2/HO-1 may be employed as a target for neuroprotection after ICH.

Lateral Craniopharyngeal Canal: An Anatomical Cause of Spontaneous Rhinorrhea.

The aim of this report is to investigate the pathogenesis and surgical treatment of encephalocele located in the sphenoid sinus and presented with spontaneous rhinorrhea. The data of a patient with sphenoid sinus encephalocele was analyzed in association with the review of literature. The patient admitted to our clinic with rhinorrhea from the left nasal cavity. Cranial magnetic resonance imaging revealed bone defects in the left sphenoid sinus wall, and the presence of brain tissue and cerebrospinal fluid (CSF) in the sphenoid sinus. The patient underwent dural repair via left pterional approach. Rhinorrhea disappeared after surgery. The pathogenesis of the encephalocele in the sphenoid sinus is not clear. It may be related to the presence of lateral craniopharyngeal canal, extra-gasification in the sphenoid sinus, high intracranial pressure or other factors. It is very important to diagnose accurately the source of CSF fistula in preoperative period, choose the specific operation technique, and follow-up the patient for a long time period.

MRI research of diaphragma sellae in patients with pituitary adenoma.

This study is to investigate the clinical significance of diaphragma sellae in patients with pituitary adenoma by MR images. A total of 47 cases of pituitary adenoma patients were enrolled in this study. Preoperative and postoperative MR scanning together with preoperative 3D-GE sequential scanning were performed. A series of parameters of diaphragma sellae were measured and compared. Tumor height was greater in patients with convex diaphragma sellae than that in patients with concave diaphragma sellae. The width and height of diaphragmal opening were positively related to tumor height. Diaphragmal opening width in the invasive group was greater than that of the non invasive group. Diaphragmal opening width in the non total resection group was significantly greater than that in the total resection group. Tumor resection rate was negatively correlated to diaphragmal opening width in the non total resection group. Lift angle of bilateral epidural around diaphragmal opening was positively related to tumor height. Enhanced 3D-GE images can perfectly display diaphragma sellae and parameters of tumor height and tumor invasiveness are related to diaphragmal opening diameter.

Anatomy and CT reconstruction of the anterior area of sphenoid sinus.

BACKGROUND: The anatomical structures of anterior area of sphenoid sinus are observed by CT reconstruction of radiographic images in some studies. However, the detailed anatomic information of the extended transsphenoidal approach is still incomplete. METHOD: Fifteen cases (30 sides) of adult cadaveric skulls and 20 cases (40 sides) of bleached adult dry skulls were observed and measured under microscope. CT imaging data were obtained from 12 patients. RESULTS: Anatomy of anterior area of sphenoid sinus and sphenopalatine artery observed from CT three-dimensional reconstructed images was consistent with that observed from adult cadaveric skulls and bleached adult dry skulls. The anterior sphenoid sinus wall resembled a bird head, with midline protrude prismatically. The sphenoid ostia on both sides were in shape of bird-eyes, and the sphenoidal rostrum below was like the beak. The "shallowest point" was firstly reported in this study and was defined as the nearest point from the nostril to the anterior sphenoid sinus wall. It was located about 5.5 mm from sphenoid sinus ostium, and 5 mm from the upper edge of the posterior choanae. It was an important anatomical reference mark in locating the sphenoid sinus ostium in the anterior sinus wall. CONCLUSION: The three-dimensional images reconstructed by CT scan can visually display the bone structure of anterior area of sphenoid sinus, sphenopalatine artery and its main branches. Virtual endoscopy reconstruction can confirm the structural details of CT reconstruction and simulate transsphenoidal surgery.

Anatomic study and clinical significance of extended endonasal anterior skull base surgery.

OBJECTIVE: This study is to investigate the anatomical relationship of endonasal approach for anterior skull base surgery, and to determine the boundaries between anterior basicranial craniotomy and the security of operative techniques. MATERIALS AND METHODS: A total of 10 adult dry skulls and 13 adult cadaveric heads processed by formalin were examined under operating microscope. The micro-anatomic structures of the turbinate, sphenoid sinus, ethmoid sinus, anterior ethmoidal artery, posterior ethmoidal artery and anterior skull base were observed. Artificial anatomy was performed and the deep-seated regions of the surgical approach were observed under operating microscope and endoscope. RESULTS: Examined from the intracranial and intranasal aspects, it was found that the middle turbinate, uncinate process, ethmoid bulla, lamina papyracea, anterior ethmoid canal, posterior ethmoid canal, prominence of the optic canal and opticocarotid recess were all important anatomic landmarks for surgery. The horizontal distances between medial orbital wall on both sides at the level of crista galli, anterior ethmoid canal, and posterior ethmoid canal were (22.31 ± 3.08) mm, (23 ± 2.93) mm, and (26.25 ± 2.88) mm, respectively. The distance between the double optic canal cranial opening was (14.67 ± 3.82) mm. CONCLUSIONS: During the endonasal approach for anterior skull base surgery, full advantage of the surgical corridor made by the middle turbinate resection should be taken. To control intraoperative bleeding, it is critical to identify anterior and posterior ethmoidal artery. Identification and protection of medial orbital wall and the optic nerve, and controlling the ranges of anterior basicranial craniotomy are of great importance for surgical safety.

A new design of robust H∞ sliding mode control for uncertain stochastic T-S fuzzy time-delay systems.

In this paper, a novel dynamic sliding mode control scheme is proposed for a class of uncertain stochastic nonlinear time-delay systems represented by Takagi-Sugeno fuzzy models. The key advantage of the proposed scheme is that two very restrictive assumptions in most existing sliding mode control approaches for stochastic fuzzy systems have been removed. It is shown that the closed-loop control system trajectories can be driven onto the sliding surface in finite time almost certainly. It is also shown that the stochastic stability of the resulting sliding motion can be guaranteed in terms of linear matrix inequalities; moreover, the sliding-mode controller can be obtained simultaneously. Simulation results illustrating the advantages and effectiveness of the proposed approaches are also provided.