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Objective: To investigate the effects of leptin on glucose metabolism and related inflammatory factors in diabetic rats. Methods: Ten healthy male Wistar rats were randomly selected as the control group. Fifty rats were fed with high sugar and high fat diet and injected with streptozotocin (STZ, 25 mg/kg) intraperitoneally. They were randomly divided into model group, leptin low, middle and high dose group. The rats in the low, middle and high dose group were fed with leptin at the doses of 20, 50 and 100 μg/kg for 5 d respectively. Blood glucose (FBG) was measured by GOD-PAP method, insulin content (INS) was tested by radioimmunoassay, the serum levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C) were determined by automatic biochemical analyzer, the contents of malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). Western blot was used to detect the expression of leptin in adipose tissue of diabetic rats. Results: Compared with the control group, the blood glucose levels of other groups were increased significantly (P＜0.01). Compared with the model group, the blood glucose levels of middle and high dose leptin rats decreased significantly (P＜0.05, P＜0.01). The insulin level of high dose leptin group decreased significantly (P＜0.01). There was no significant difference in FBG and INS among the three groups (P＞0.05). Compared with the model group, TC levels of middle and high dose leptin group were decreased significantly (P＜0.05, P＜0.01). TG and LDL-C levels of high dose leptin group were decreased significantly (P＜0.05), HDL-C level of high dose group was increased significantly (P＜0.01). Compared with different dose groups, the high dose of leptin (100 μg/kg) could decrease the levels of TC, TG and LDL-C, and increase the level of HDL-C, which was better than those of the middle and low dose of leptin (P＜0.05) Compared with the model group (52.27±10.93), the levels of leptin in low, middle and high dose group were (47.35±12.09), (44.68±10.23) and (40.13±9.87) respectively, which could be decreased by leptin in a dose-dependent manner. Conclusion: The abnormal secretion of leptin is one of the factors inducing diabetes mellitus. Under the intervention of a certain concentration of exogenous leptin (100 μg/kg), it can significantly reduce the level of MDA, TNF-α, and improve the level of IL-6. The mechanism may be closely related to the reduction of inflammatory response, oxidative stress and correction of dyslipidemia. Leptin also reduces the risk of disease progression in diabetes treatment.

Objective: The aim of this study is to analyze the effects of glutathione on oxidative stress, leptin and adiponectin in patients with obstructive sleep apnea（OSA） complicated with metabolic syndrome. Method: One hundred and fifty-nine patients with OSA and MS were enrolled in the group A according to the exclusion criteria. One hundred and fifty-nine patients with MS group were not included in the OSA group, and 159 patients were included in the control group. Before and after treatment, the levels of serum malondialdehyde （MDA）, superoxide dismutase （SOD）, Leptin and ADP were respectively detected, and the clinical effects of the three groups were compared. Result: Compared with the control group, the contents of MDA and Leptin in the case A and B groups were significantly higher than that of the control group, and the contents of SOD and ADP were significantly lower than that of the control group, and the difference was statistically significant, especially in case group A. The level of SOD and ADP was significantly higher in the group after treatment than before treatment, and the level of MDA and Leptin was significantly lower than before treatment. The difference was statistically significant, especially in case group A, too. Conclusion: Patients with OSA and MS are associated with oxidative stress. Glutathione can effectively improve the body's ability to resist oxidative stress, reduce oxidative damage, reduce leptin, and increase ADP levels., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Objective: To observe the expression of leptin (LP) and its influence on pulmonary fibrosis in experimental rats with silicosis and the correlation between the expressions of leptin and HIF-1α., Methods: A total of 120 male Sprague-Dawley rats were randomly divided into normal control group, silicosis model group, LP intervention groups (consisting of LP5, LP10 and LP20 groups according to the concentration of LP). The rats in the normal control group were intratracheally administered 1 mL normal sodium, and the ones in the other groups were intratracheally given 1 mL SiO₂(40 mg/mL) suspension. The rats in LP intervention groups were intraperitoneally injected with leptin 5, 10, 20 ng/kg.d respectively from the first day. Six rats in each group were sacrificed on the 7th, 14th, 21th and 28th day. The expression of LP on the 7th, 14th, 21th and 28th day and the hydroxyproline content on the 28th day in rat lung tissues were measured by ELISA, and the expressions of HIF-1α and LP proteins in the lung tissues of the silicosis model group were measured by Western blotting., Results: There were significant differences in the expression of LP in the lung tissues at each time point (7th, 14th, 21th and 28th day) among the five groups (F=669.18, 948.67, 1 172.00, 521.55, P<0.05). The LP content in the silicosis model group was significantly higher than that in the normal control group (P<0.05) and the expression of LP in the LP intervention groups were significantly elevated at each time point (P<0.05) as compared with the silicosis model group. Hydroxyproline content on 28th day was (0.89 ± 0.16), (3.14 ± 0.40), (3.78 ± 0.27), (4.35 ± 0.13), (4.87 ± 0.16) mg/g in normal control group, silicosis model group, LP5, LP10 and LP20 intervention groups, respectively. Compared with the normal control group, hydroxyproline content in the silicosis model group significantly increased (P<0.05), and compared with the silicosis model group, hydroxyproline content in LP intervention groups were significantly raised (P<0.05). The significant positive correlations were noted between the expressions of HIF-1α and LP (r=0.876, 0.796, 0.859 and 0.854 at each time, P<0.05)., Conclusion: The expression of LP goes up significantly in the lung tissues of rats with silicosis. Addition of exogenous leptin can increase the collagen deposition in the lung tissues; meanwhile leptin has a positive correlation with HIF-1α.

Objective: To investigate the effect of topical application of leptin in promoting burn wound healing in rats., Methods: Four parallel second-degree burn wounds induced on the back of 18 Wistar rats were divided into leptin treatment group (treated with topical application of 400 ng/ml leptin dissolved in PBS) and control group (treated with PBS). The time of wound healing was recorded, and the wound area that was not healed was measured at 3, 7, 11, 15, and 19 days after burns. The tissue at the peripheries of the wound was sampled at 7, 14 and 21 days after burns for pathological examination with HE staining and immunohistochemistry for proliferating cell nuclear antigen (PCNA) to evaluate the proliferation of keratinocytes., Results: Compared with the control group, leptin-treated wounds showed a shorter time (by 2-3 days) of wound healing, and significant differences were found between the two groups in healing at 7, 11, 15, and 19 days after burns. HE staining and immunohistochemistry revealed a faster rate of epidermis growth and a greater thickness of the cuticular layer in leptin-treated wounds at 7, 14 and 21 days after burns. PCNA positivity in the keratinocytes was stronger in leptin-treated wounds than in the control wounds at 7 and 14 days, but no such distinct difference was noted at 21 days between the two groups., Conclusion: Topical application of leptin can promote re-epithelization in burn wounds to shorten the wound healing time of burns.

Objective: To investigate the effect of leptin on collagen systhesis in wounded rats., Methods: Thirty male Wistar rats, weight (180 +/- 20)g, were randomly divided into three groups (n = 10) by weight: normal depilation group, wound control group and leptin treatment group and ten rats were included in each group. A full-thickness defect measuring 2 x 2.5 cm was made in the back of rats in wound control group and leptin treatment group. Each wound in rats of leptin treatment group was applied topically with 0.1 ml leptin solution (2.0 microg leptin), daily for 7 days and that of wound control group with equivalent saline solution. All rats were killed and then granulation tissues samples and skin were collected to examine the synthesis of collagen., Results: Hydroxyproline content in granulation tissues of in leptin treatment group (33.92 +/- 3.09) mg/g were significantly increased than those in control group (29.55 +/- 3.59 mg/g, P < 0.05). The mRNA expressions of collagen I and III were significantly enhanced in leptin treatment group (0.96 +/- 0.09, 0.09 +/- 0.06) than those in control group (0.80 +/- 0.03, 0.08 +/- 0.03). The levels of type I and III collagen were significantly increased in leptin treatment group than those in control group., Conclusion: Leptin applied topically can accelerate wound healing through enhancing gene expression of type I and III collagen and synthesis of collagen in wound tissue.

Background & Objective: Epidemiologic studies showed that leptin is closely related to the tumorigenesis of endometrial cancer, but the mechanism is unclear. As a mitogenic agent, leptin can promote the proliferation of many kinds of cells. This study was to explore the role of extracellular signal-regulated kinase 1/2 (ERK1/2) in leptin promoting the proliferation of human endometrial cancer cell line Ishikawa., Methods: The expression of leptin receptor OB-Rb in Ishikawa cells was detected by fluoroimmunoassay. Ishikawa cells were treated by leptin at various concentrations (0, 10, 50, 100, and 150 ng/ml) for different time (6, 12, and 24 h). Cell proliferation was examined by MTT assay. Meanwhile, the effect of PD98059, selective inhibitor of ERK1/2, on the proliferation of Ishikawa cells induced by leptin was also studied. Ishikawa cells were treated with 100 ng/ml leptin for different time (20, 40, and 60 min), then the levels of phosphorylated ERK1/2 (p-ERK1/2) and ERK1/2 were examined by Western blot., Results: Fluoroimmunoassay showed the presence of OB-Rb in Ishikawa cells. Leptin stimulated the proliferation of Ishikawa cells. This effect was maximal at 100 ng/ml after 24-hour treatment, and there was no significant difference between 100 ng/ml group and 150 ng/ml group (P=0.129). Blocking ERK1/2 phosphorylation by PD98059 significantly reduced the proliferation of Ishikawa cells stimulated by leptin. When treated with 100 ng/ml Leptin and 100 micromol/L PD98059 for 24 h, cell proliferation rate was (6.88+/-0.86)%. ERK1/2 phosphorylation was enhanced significantly in Ishikawa cells after treatment of 100 ng/ml leptin., Conclusion: Leptin may promote the proliferation of endometrial cancer Ishikawa cells by activating ERK1/2 signaling pathway.