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AIM:To establish a mouse model of immuno-inflammation in central nervous system (CNS) associated with cognitive dysfunction.METHODS:C57BL/6J male mice were divided into 3 groups.Lipopolysaccharide (LPS) was intraperitoneally injected into the mice to induce cognitive impairment.Morris water maze test, passive avoidance test and pole test were used to observe the behavioral changes of mice.The histomorphology was analyzed by the method of immunofluorescence.The detailed molecular mechanism was determined by Western blot.RESULTS:Compared with saline group, LPS induced mouse sickness behavior and memory loss.Microglia activation and neuronal loss in the hippocampus were observed.The expression of neuroinflammatory proteins COX-2 and iNOS in the brain of LPS-induced mice was increased.CONCLUSION:Intraperitoneal injection of LPS induces cognitive dysfunction in mice.
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AIM:To screen and verify the effective ingredient of traditional Chines medicine (TCM) Q0409 in improving learning and memory ability of mice.METHODS:The mouse learning and memory impairment model was induced by intraperitoneal injection of scopolamine.The mice in each group were given the corresponding drug by gavage at the same time for 14 d in succession.Morris water maze test was used to measure the learning and memory ability of the mice, and then the hippocampal tissue homogenate was taken to determine the activity of acetylcholinesterase (AChE).The animals were divided into 8 groups according to L8(27) orthogonal table.The variance analysis and factorial analysis were used to analyze the pharmacological effects of seven kinds of single herbal in TCM Q0409 and determine the screening ingredients.The animals were divided into 6 groups according to the results of the preliminary screening results, and further testing and validation of TCM Q0409 screening ingredients were performed to get the final simplified ingredients.RESULTS:Three medicinal herbs of Polygalae, Panax ginseng and Acori graminei rhizome were screened by the orthogonal results of Morris water maze test and the activity of AChE in mouse hippocampal tissues.The simplified ingredients of TCM Q0409 were obtained through the variance results of Morris water maze test and the activity of AChE in mouse hippocampal tissues.CONCLUSION:Polygala and ginseng were eventually determined as simplified ingredients of TCM Q0409 and it was verified that they improve the learning and memory ability of the mice with learning and memory impairment.
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AIM:To investigate the protective effect of lycopene on primary mouse cerebrocortical neurons ex -posed to tert-butyl hydroperoxide ( t-BHP) and its mechanisms of in vitro.METHODS:Primary cerebrocortical neurons of newborn C57 mice were extracted and divided into normal group , t-BHP group, lycopene +t-BHP group and lycopene group.The neuronal damage was induced by t-BHP exposure for 24 h, and the cell viability was examined by MTT assay . ROS content was measured by flow cytometry , and the protein levels of Bax , Bcl-2, caspase-3, cleaved caspase-3 and cyto-chrome C were examined by Western blot .RESULTS:The primary mouse cortical neurons expressed MAP-2 protein.Ly-copene at concentration of 4μmol/L reversed the decrease in cell viability .Flow cytometry revealed that lycopene treatment attenuated ROS content under the condition of t-BHP exposure.In addition, the protein level of Bcl-2 was increased, and the expression of Bax , cleaved caspase-3 and cytochrome-C was suppressed in lycopene +t-BHP group.CONCLUSION:The protective effect of lycopene on cortical neurons with t-BHP-induced injury may be involved in the mechanism of neuro-nal antioxidative response by down-regulating caspase-3 and Bax/Bcl-2 through the mitochondrial apoptotic pathway .
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AIM: To observe the effects of berberine (Ber) on enterocyte apoptosis in septic mice and its pos-sible mechanism.METHODS: Male C57BL/6 mice (8 ~10 weeks old) were randomly divided into sham group, cecal ligation and puncture (CLP) group, CLP +Ber group and sham +Ber group.The mice in CLP group underwent CLP ope-ration, and the mice in sham groups suffered a similar operation except the ligation and puncture.After the sham or CLP operation, the mice were administered intragastrically with distilled water or berberine (50 mg/kg) within 2 h.After 20 h, the mice were killed with excess pentobarbital sodium and the ileum tissues were removed.The histological changes of the intestine were observed and the enterocyte apoptosis was examined by determining the protein level of cleaved caspase-3. Furthermore, mitochondrial Bax, cytoplasm cytochrome C (Cyt C) and the total proteins of Bcl-2, Fas, FasL and Fas-as-sociated protein with death domain (FADD) were examined by Western blot.The mRNA expression of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) was measured by real-time PCR.RESULTS: The extensive ileum injuries, including remarkably increased leukocytes and necrosis of intestinal villus were observed 20 h after CLP.In CLP group, the protein levels of cleaved caspase-3, cytoplasm Cyt C, as well as Fas, FasL were significantly increased, but the Bcl-2 level was decreased.Bax translocation into mitochondria was promoted.However, FADD was not changed significantly.The mRNA expression of TH and DBH was also increased sharply in CLP group.On the contrary, treatment with berberine made a considerable alleviating alteration in the ileum of the septic mice.CONCLUSION: Treatment with berberine pro-vides protective effects on intestinal injury in septic mice by reducing enterocyte apoptosis, and its possible mechanism may be involved in the inhibition of the endogenous and exogenous apoptosis pathways.
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AIM:To study the expression of glycine receptorα1 subunit in neonatal rat myocardial cells and to investigate the effect of lipopolysaccharide (LPS), hypoxia/reoxygenation, isoproterenol (ISO) and high concentration of glucose (HG) on the expression of glycine receptorα1 subunit in the neonatal rat myocardial cells.METHODS:Neonatal rat myocardial cells were cultured in vitro.The expression of glycine receptorα1 subunit was detected by Western blotting. The neonatal rat myocardial cells were treated with LPS (20 mg/L), ISO (100 μmol/L) or high concentration of glucose (25 mmol/L) for 24 h, or were exposed to hypoxia for 3 h followed by reoxygenation for 3 h.Subsequently, the cell viabil-ity was measured by CCK-8 assay, and the expression of glycine receptorα1 subunit was determined by Western blotting. RESULTS:The expression of glycine receptor α1 subunit in the neonatal rat myocardial cells was positively detectable by Western blotting.Compared with control group, no significant difference of the cell viability ( P>0.05) in LPS group, ISO group, hypoxia/reoxygenation group and HG group was observed.The expression of glycine receptor α1 subunit was in-creased (P<0.01) in LPS group, ISO group and hypoxia/reoxygenatio group, but decreased (P<0.01) in HG group. CONCLUSION:Glycine receptorα1 subunit exists in the neonatal rat myocardial cells.A certain concentration of LPS or ISO, or hypoxia/reoxygenation for a certain period upregulate the expression of glycine receptorα1 subunit, but HG down-regulates the expression of glycine receptor α1 subunit in cultured neonatal rat myocardial cells.
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AIM:To observe the effect of B-HT933, a selective α2-adrenoceptor agonist, on lipopolysaccha-ride ( LPS )-induced TNF-αproduction in neonatal rat cardiomyocytes and to explore the underlying mechanisms . METHODS:The neonatal rat cardiomyocytes were cultured .The localization of α2A-adrenoceptor in the cardiomyocytes was examined by immunofluorescence staining .The cardiomyocytes were exposed to LPS or/and B-HT933 for different time.The level of TNF-αin the supernatants and the mRNA expression of TNF-αwere detected by ELISA and real-time PCR, respectively.In addition, LPS-associated signal molecules in the cardiomyocytes were also examined by Western blotting.RESULTS: Immunofluorescence staining showed that α2A-adrenoceptors were localized in the cardiomyocytes . LPS stimulated TNF-αproduction in the cardiomyocytes in a dose and time-dependent manner .B-HT933 pretreatment sig-nificantly inhibited the expression of TNF-αat mRNA and protein levels in LPS-treated cardiomyocytes .Furthermore, LPS exposure induced IκBαand p38 phosphorylation in cardiomyocytes and only IκBαphosphorylation was prevented by B-HT933 treatment.CONCLUSION:α2A-adrenoceptors are present in neonatal rat cardiomyocytes and its agonist B -HT933 inhibits LPS-induced TNF-αproduction in cardiomyocytes via suppressing IκBαphosphorylation .
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[ ABSTRACT] AIM:To explore the role of Huoxue Jiangzhi Recipe in preventing and treating fatty liver in mice and its underlying mechanisms.METHODS:Healthy Kunming mice were fed with high-fat diet and treated intragastrically with different doses of Huoxue Jiangzhi Recipe ( compound of ginseng, panax notoginseng and rhizoma gastrodiae, named as GST) for 2 weeks.The levels of blood lipids and triglyceride ( TG) in hepatic tissues were measured.Meanwhile, liver in-dex and hepatic pathology were observed.The optimized dosage of Huoxue Jiangzhi Recipe was determined by the experi-ments.The mice were divided into normal control group ( NC group, fed with normal diet) and model group ( fed with high-fat diet) .The model mice were subdivided into 3 subgroups 12 weeks later:HF group ( fed continuously with high-fat di-et) , ND group ( fed with normal diet) , GSL group ( fed with normal diet and treated intragastrically with GSL) .The mice in NC, HF and ND groups were given distilled water by gastric perfusion.Two weeks later, all mice were killed, and blood was collected for measuring serum total cholesterol (TC),TG,high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol ( LDL-C) contents, hepatic TC, TG, malondialdehyde ( MDA ) levels and superoxide dismutase ( SOD) activity were detected.Moreover, liver index and hepatic pathology were also observed.The mRNA expression of peroxisome proliferator-activated receptor alpha (PPARα) and cytochrome-P450 2E1 (CYP2E1) in the liver was examined by RT-PCR.RESULTS:GST significantly decreased serum lipid, hepatic lipid and MDA levels and elevated SOD activi- ty.Furthermore, GST markedly reduced liver index, improved hepatic adipose infiltration, increased PPARαmRNA ex-pression and inhibited CYP2E1 mRNA expression.CONCLUSION:GST is effective in the treatment of fatty liver in mice by up-regulating PPARα, thus reducing serum and hepatic TG levels, down-regulating CYP2E1 and inhibiting lipid peroxi-dation.
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[ ABSTRACT] AIM:To observe the effects of berberine and yohimbine on splenocyte apoptosis in septic mice and underlying mechanisms.METHODS:The mice were subjected to cecal ligature and puncture ( CLP) .The drugs or vehi-cle were given intragastrically 2 h after the surgery according to the following 5 groups:sham, CLP, CLP+berberine, CLP+yohimbine, and CLP+berberine+yohimbine.The apoptosis of splenocytes stained by TUNEL was observed under laser scanning confocal microscope 20 h after CLP.The splenic lymphocytes were isolated and observed using flow cytometry. The activities of caspase-3, caspase-8 and caspase-9 in splenic lymphocytes were detected, and the expression of Fas, Bim, Bcl-2 and Bax in the splenocytes was also determined by Western blotting.RESULTS:The TUNEL staining showed that the apoptotic rate of the splenocytes in septic mice 20 h after CLP was significantly higher than that in sham and CLP+yohimbine groups (P<0.05).Compared with CLP group, the proportion of apoptotic cells was decreased in septic mice in CLP+berberine+yohimbine and CLP+yohimbine groups ( P<0.05) .Flow cytometry analysis demonstrated the similar results in the apoptosis of splenocytes and T lymphocytes.However, only yohimbine treatment reduced the apoptosis of B lymphocytes in the spleen of sepsis-challenged mice.Compared with CLP group, caspase-9 activity was significantly re-duced in CLP+berberine group (P<0.05), the activities of caspase-3, caspase-8 and caspase-9 were all statistically re-duced (P<0.05) in CLP+yohimbine group and CLP+yohimbine+berberine group.CLP significantly increased the ex-pression of cytosolic Fas, Bim and mitochondrial Bax in the splenocytes, and decreased Bcl-2 expression compared with sham group.Compared with CLP group, the expression of cytosolic Bim and mitochondrial Bax in CLP+berberine group were reduced (P<0.05).Fas expression decreased only in CLP+yohimbine group (P<0.05).Berberine combined with yohimbine reduced the expression of cytosolic Fas, Bim and mitochondrial Bax in the septic mouse splenocytes ( P <0.05).CONCLUSION:Yohimbine reduces sepsis-induced splenic lymphocyte apoptosis in mice by inhibiting Fas expres-sion and in turn blocking both extrinsic and intrinsic apoptosis pathways.Berberine reduces Bim expression and inhibits caspase-9 activation, but not caspase-3 activation and apoptosis in the septic mouse splenocytes.Berberine combined with yohimbine reduces splenocyte apoptosis in the septic mice by inhibiting both extrinsic and intrinsic apoptotic pathways.
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AIM:To explore the preliminary mechanism of senegenin ( Sen) on inhibiting hypoxia/reoxygenation ( H/R)-induced apoptosis of primary cortical neurons .METHODS:The cultured cortical neurons were randomly divided in-to normal group (control group), model group (H/R group), Sen+H/R group and Sen group.Flow cytometry was used to evaluate the effect of Sen on H/R-induced cell apoptosis .The protein levels of JNK , p-JNK, c-Jun, p-c-Jun, Bcl-2 and Bax were assessed by Western blotting .RESULTS:The apoptotic rate in H/R group was obviously higher than that in control group (P<0.05), while the apoptotic rate in Sen +H/R group was obviously lower than that in H/R group (P<0.05), suggesting that the model of apoptosis was established successfully .The results of Western blotting showed that Sen increased the expression of JNK and c-Jun, inhibited the phosphorylation of JNK and c-Jun (P<0.05), increased the protein level of Bcl-2 and inhibited the protein level of Bax in H/R treated primary cortical neurons (P<0.05).CONCLUSION:Sen has a protective effect against H/R-induced neuronal apoptosis by increasing the expression of JNK and c-Jun, inhibiting the phosphorylation of JNK and c-Jun, increasing the protein level of Bcl-2 and decreasing the protein level of Bax .
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AIM:To investigate the effects of thalidomide ( THD) on the activation of connective tissue growth factor ( CTGF) gene promoter induced by transforming growth factor β1 ( TGF-β1 ) in human embryonic lung fibroblasts ( HELF) .METHODS:DNA sequence of CTGF gene promoter was cloned into luciferase reporter gene vector to construct the recombinant eukaryotic expression vector pGL 3-CTGFP, and the recombinant vector was transfected into HELF cell line.The effects of TGF-β1 and THD on the activation of CTGF gene promoter were detected by dual-luciferase analysis . RESULTS:TGF-β1 increased the reporter gene activity dose-dependently (P<0.05), with a plateau at 5 μg/L being 2.16 folds as high as the control .TGF-β1-induced increase in the reporter gene activity was also time-dependent ( P<0.05).After exposure to TGF-β1(5 μg/L), the level of luciferase activity reached its peak at 12 h and was 2.52 folds as high as the control .THD significantly inhibited TGF-β1-induced increase in the reporter gene activity in a dose-dependent manner , but its basal activity was not changed .CONCLUSION: TGF-β1 stimulates the transcriptional activity of CTGF gene promoter in HELF cells in a dose-and time-dependent manner , while THD may inhibit the effects dose-dependently .
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RNA interference(RNAi)is a process by which introduced small interfering RNA(siRNA)can cause the specific degradation of mRNA with identical sequences. The human herpes simplex virus type 1(HSV-1)RR is composed of two distinct homodimeric subunits encoded by UL39 and UL40, respectively. In this study, we applied siRNAs targeting the UL39 and UL40 genes of HSV-1. We showed that synthetic siRNA silenced effectively and specifically UL39 and UL40 mRNA expression and inhibited HSV-1 replication. Our work offers new possibilities for RNAi as a genetic tool for inhibition of HSV-1 replication.
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Herpes simplex virus type 1 (HSV-1) is a commonly occurring human pathogen worldwide. There is an urgent need to discover and develop new alternative agents for the management of HSV-1 infection. Tripterygium hypoglaucum (level) Hutch (Celastraceae) is a traditional Chinese medicine plant with many pharmacological activities such as anti-inflammation, anti-tumor and antifertility. The usual medicinal part is the roots which contain about a 1% yield of alkaloids. A crude total alkaloids extract was prepared from the roots of T. hypoglaucum amd its antiviral activity against HSV-1 in Vero cells was evaluated by cytopathic effect (CPE) assay, plaque reduction assay and by RT-PCR analysis. The alkaloids extract presented low cytotoxicity (CC_(50) = 46.6 μg/mL) and potent CPE inhibition activity, the 50% inhibitory concentration (IC_(50)) was 6.5 μg/mL, noticeably lower than that of Acyclovir (15.4 μg /mL). Plaque formation was significantly reduced by the alkaloids extract at concentrations of 6.25 μg/mL to 12.5 μg/mL, the plaque reduction ratio reached 55% to 75% which was 35% higher than that of Acyclovir at the same concentration. RT-PCR analysis showed that, the transcription of two important delayed early genes UL30 and UL39, and a late gene US6 of HSV-1 genome all were suppressed by the alkaloids extract, the expression inhibiting efficacy compared to the control was 74.6% (UL30), 70.9% (UL39) and 62.6% (US6) respectively at the working concentration of 12.5μg/mL. The above results suggest a potent anti-HSV-1 activity of the alkaloids extract in vitro.
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AIM: To establish the cell model of hippocampal neurons impaired by the supernatant of microglia conditioned medium (MCM) induced by LPS, and to study the mechanisms of neuron damage and the protection effect of curcumin. METHODS: The microglia were activated and stimulated by LPS at concentration of 5 μg/L. The supernatant of activated MCM was used to stimulate the hippocampal neurons. The morphology of the neurons was observed under light microscope and the survival rate was detected by MTT. The availability of respiration in the hippocampal neurons was determined by detecting the ratio of lactic acid/pyruvic acid, and the expression of 3 types of 1,4,5-inositol triphosphate (IP3R1, IP3R2, IP3R3) was detected by RT-PCR. RESULTS: The hippocampal neurons were damaged severely by the supernatant of activated MCM, and the morphology of the neurons changed significantly. Compared to control group, the ratio of lactic acid/pyruvic acid in MCM group was elevated and the expression levels of IP3R1 and IP3R3 in the hippocampal neurons were significantly increased. The ratio of lactic acid/pyruvic acid and the expression of IP3R1 in curcumin+MCM group were evidently lower than those in MCM group. However, no effect of curcumin on IP3R3 expression was observed, the changes of neural morphology was also ameliorated in curcumin+MCM group. CONCLUSION: Curcumin protects rat hippocampal neurons from damage induced by LPS-induced microglia condition medium.
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AIM:Scopolamine blocks cholinergic transmission and impairs learning and memory in mice．The purpose of this study was to evaluate the memory-improving properties of curcumin on scopolamine-induced memory im-pairment in mice．METHODS：The mice of memory impairment were induced by scopolamine．Step down test and Morris water maze test were used to observe the earning and memory ability in curcumin-treated ice．Biochemical assessments of AChE，MDA，and GSH-Px levels in brains were performed．RESULTS：Oral administration of curcumin ignificantly reduced the numbers of step-down rrors(P<0．05)and prolonged the step-down latency induced by scopolamine(P<0．05)．The escape latency time in mice treated with curcumin Was remarkably educed compared to that in scopolamine group by Morris water maze test(P<0．05)．After the platform was removed，the total time that the mice swam in the tar-get quadrant Was also longer in curcumin group than that in model group(P<0．05)．The data also indicated that curcumin significantly inhibited AChE ctivity(P<0．01)and prevented oxidative stress characterized by the significant reduction in MDA content and the significant increase in GSH-Px activities in the brain(P<0．01)．CONCLUSl0N：Curcumin in-duces cognitive improvement by enhancing the function of cholinergic system and its antioxidant activity．
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Abstract］ AIM and METHODS:The recent work from our laboratory showed that ventral septal area (VSA) played a negative-regulatory central role in thermoregulation during endogenous pyrogen-induced fever. In order to further investigate the role of VSA in the antipyretic mechanism, we observed the effects of electrical stimulation of VSA on firing characteristics of thermosensitive neurons in preoptic anterior hypothalamus (POAH) by using extracellular microelectrode technique on 32 New Zealand white rabbits treated with interleukin-1 β (IL-1β) intracerebroventriculary (ICV). RESULTS:(1)Injection of IL-1β decreased discharging rate of warm-sensitive neurons in POAH. Electrical stimulation of VSA remarkably decreased thermosensitive coefficient of warm-sensitive neurons. (2)Injection of IL-1β caused increase in discharging rate of cold-sensitive neurons in POAH. Electrical stimulation of VSA remarkably increased thermosensitive coefficient of cold-sensitive neurons. CONCLUSTION:VSA may have an antipyretic effect through affecting the firing characteristics of thermosensitive neurons in POAH during IL-1β-induced fever.
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The primary action of corticotropin releasing hormone (CRH) is stimulation of the synthesis and release of adrenocorticotropic hormone and β-endorphin from the pituitary in response to stress. In addition, a number of studies indicate that CRH exerts other physiological actions within the central nervous system which are independent of the pituitary. These include increased body temperature and thermogenesis. However, the intracellular mechanism responsible for pyrogenic action of CRH is still unclear. The purpose of these studies was to determine whether or not cAMP was involved in the pyrogenic action of CRH in the rat. Intracerebroventricular (icv) microinjection of CRH (2.5 μg, 5.0 μg, 10 μg) caused increases in colonic temperature and hypothalamus cAMP level in conscious rats. The pyrogenic effects of CRH were abolished or markedly inhibited by prior injection (icv) of an adenylate cyclase inhibitor, 2，，3，-dideoxyadenosine (DDA, 30 μg) or an inhibitor of cAMP-dependent protein kinase, adenosine-3，，5，-(cyclic) monophosphorothionate (Rp-cAMPs, 15 μg). This is the first report demonstrating the pyrogenic effcet of centrally administration of CRH on the rat via the cAMP-mediated protein kinase signal transduction pathway.
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AIM and METHODS:To investigate the effect of electrical stimulation of VSA on the firing of thermosensitive neurons in preoptic anterior hypothalamus (POAH), the firing rate of thermosensitive neurons in POAH of 20 New Zealand white rabbits was recorded by using extracellular microelectrode techinque. RESULTS:(1)Electrical stimulation of ventral septal area (VSA) caused a significant increase in firing rate of warm-sensitive neurons in the preoptic area of the anterior hypothalamus(POAH).(2) The firing rate of cold-sensitive neurons was decreased remarkably in the POAH by electrical stimulation of VSA. CONCLUSION:VSA may play a controlling role in the thermoregulation through altering the firing rate of thermosensitive neurons in the POAH.
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AIM: To investigate the mechanisms by which siduqing, a Chinese medicine, protects against lipopolysaccharide (LPS)-induced acute renal dysfunction. METHODS: Mice were divided randomly into control, LPS, siduqing treatment and siduqing groups, and treated intragastrically with siduqing at a dose of (1 000) g/L (0.2 (mL/10 g) body weight) or distilled water (0.2 (mL/10) g body weight) twice a day for 3 days, LPS (30 mg/kg) or normal saline was injected intraperitoneally on day 3, followed by intragastrical administration with siduqing at a dose of (1 000) g/L (0.2 (mL/10 g) body weight) or distilled water (0.2 (mL/10 g) body weight). Blood was collected for determining urea nitrogen (BUN) and creatinine (Cr) contents, renal tissue for examining superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. In addition, electron microscopy was used to examine the ultrastructure changes in kidney, and RT-PCR was performed to detect renal intercellular adhesion molecule-1 (ICAM-1) mRNA expression. RESULTS: LPS significantly increased serum urea nitrogen (BUN) and creatinine (Cr) contents, and produced an obvious pathological change in renal ultrastructure, which were significantly attenuated by siduqing treatment. Moreover, siduqing treatment increased renal SOD activity, also markedly suppressed an increase in renal MDA production and ICAM-1 mRNA expression induced by LPS. CONCLUSION: These results suggest that siduqing protects against LPS-induced acute renal injury through inhibiting ICAM-1 mRNA expression, enhancing renal SOD activity and attenuating oxidant stress.
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AIM: To study the influence of glycine(GLY) on lipopolysaccharide-binding protein(LBP) mRNA expression induced by LPS. METHODS: The level of LBP mRNA expression in liver tissues of rats was examined by RT-PCR,and the effects of glycine on LBP mRNA expression in liver tissues of rats induced by LPS were investigated. RESULTS: The level of LBP mRNA expression in hepatic tissue of rats in the LPS group was significantly higher than that in the control group( P
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Obesity is a severely public health problem the whole society faces, and it is correlated closely with many diseases, such as diabetesⅡ, hypertension, coronary heart disease,gallstone, and so on. Therefore it threatens people's survival quality severely. Obesity is a multiple-factor disease including genetic, metabolic and behavioral factor, and the gene is the main determining factor. With the development of molecular biology technique, people have founded several genes involved in obesity. Among these genes, the research on obese gene is the most profound. The protein leptin is the expression product of the obese gene. This review elucidates the structure, the main biological function, the mechanism of leptin and it's relationship with obesity.