Signal transducer and activator of transcription 3(STAT3)is known to modulate the expression of genes related to cell transformation,proliferation,and survival,making it a significant target for cancer therapy.Recent research has also highlighted the crucial involvement of aberrant STAT3 activation in the pathogenesis of diabetic kidney disease(DKD).Accordingly,this article focuses on the therapeutic potential of targeting STAT3 in DKD.The structure of STAT3,its mechanisms of activity regulation,mechanisms of abnormal STAT3 activation in DKD,and a summary of the current research is provided.The review aims provide a reference for research into the pathogenesis of DKD and the development of new drugs.

Objective:To investigate the effect of mannose on the radiosensitivity of six human non-small cell lung cancer cell lines and its possible mechanism.Methods:The expression of mannose phosphate isomerase in six lung cancer cell lines were detected by Western blot. The inhibitory effect of mannose on the proliferation of lung cancer cell lines were observed by MTT assay. When irradiated with 0, 2, 4, 6, 8 and 10 Gy, the effect of mannose on the radiosensitivity of six lung cancer cell lines was detected by plate clone formation assay, respectively; and the apoptosis rates of normal control, mannose, irradiation and combined groups were detected by flow cytometry.Results:The expression levels of mannose phosphate isomerase were different among six lung cancer cell lines. Among them, A549 cells had the highest expression level and H460 cells showed the lowest expression level. When aD ministrated with 11.1 mmol/L mannose, the same inhibitory effect was observed on both A549 and H460 cell lines. Moreover, the inhibitory effect on H460 cell line was significantly increased with the increase of mannose concentration. In addition, aD ministration of 11.1 mmol/L mannose could significantly increase the radiosensitivity and apoptosis rate of H460 cell line. However, it exerted limited effect upon the radiosensitivity and apoptosis rate of A549 cell line. Conclusion:In six lung cancer cell lines with high expression of mannose phosphate isomerase, the aD ministration of mannose can enhance the radiosensitivity of partial tumors cells.

Objective To explore the effect and mechanism of uric acid(UA)in regulating the larval growth and development of Drosophila melanogaster.Methods A total of 1350 newly hatched first-instar larvae of wild-type Drosophila melanogaster(W11 18)were collected,and the Drosophila melanogaster model of hyperurice-mia was constructed with a high purine diet.The larvae were assigned into three groups(n=150):control(stand-ard corn meal medium),low-dose adenine(corn meal medium containing 0.05％adenine),and high-dose ad-enine(corn meal medium containing 0.10％adenine),and two parallel groups were set up.The growth and de-velopment of larvae in each group was observed,and the UA and hormone levels were measured.In addition,the expression levels of genes involved in growth and development were determined.Results Compared with the con-trol group,the low-and high-dose adenine groups showed elevated UA levels(both P＜0.001)and prolonged de-velopmental period(P=0.024,P＜0.001).The high-dose adenine group showed decreased survival rate,pupa-tion rate,and eclosion rate and elevated levels of juvenile hormone(JH)and 20-hydroxyecdysone(20E)(all P＜0.001).The PCR results showed that compared with the control group,high-dose adenine upregulated the mRNA levels of reactive oxygen species(ROS),forkhead box O(FOXO),and mammalian target of rapamycin(mTOR)while downregulating the mRNA levels of Sestrin,mTOR complex 1(mTORC1),and AMP-activated protein kinase(all P＜0.001).Conclusion High concentrations of UA may promote the expression of ROS/FOXO/mTORC1/mTOR signaling pathway by regulating the levels of JH and 20E,thereby inhibiting the larval growth and development of Drosophila melanogaster.

OBJECTIVE： To investigate the protective effects of anemarsaponin B on hypoxia/reoxygenation injury astrocytes and its possible mechanism. METHODS： The primary astrocytes of neonatal SD rats were cultured and identified， and then randomly divided into normal group， model group， positive control group （nimodipine， 10 μmol/L）， anemarsaponin B low-dose， medium-dose and high-dose groups （1， 10， 100 μmol/L）， respectively. Normal group and model group were given complete medium 1 000 μL. Administration group was given complete medium with relevant medicine 1 000 μL. Except for normal group， hypoxia/reoxygenation injury model was established by oxygen-glucose deprivation/reperfusion in other groups. After reoxygenation， relative release rate of lactate dehydrogenase （LDH） in cell was detected by colorimetry. MTT assay was used to detect the relative viability of the cells. The contents of aquaporin 4 （AQP-4）， IL-6， IL-1β and TNF-α in cell were measured by ELISA. RESULTS： Compared with normal group， relative release rate of LDH， the contents of AQP-4， IL-6， IL-1β and TNF-α in cell were increased significantly in model group， while relative viability of the cells were decreased significantly （P＜0.01）. Compared with model group， relative release rate of LDH， the contents of AQP-4， IL-6， IL-1β and TNF-α in cell were decreased significantly in administration groups， while relative viability of the cells were increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： Anemarsaponin B can significantly decrease cell injury degree， strengthen cell viability and protect hypoxia/reoxygenation injury astrocytes to certain extent. The effect may be related to the down-regulation of the secretion of AQP-4， IL-6， IL-1β and TNF-α.

Objective:To investigate the possible mechanism of learning and memory damage induced by arsenic exposure through studying the effects of arsenic exposure on levels of brain-derived neurotrophic factor (BDNF) and tyrosine kinases B (TrkB) in hippocampus of offspring mice at different developmental stages.Methods:Twenty-four pregnant Kunming mice were divided into control (distilled water) group and 15, 30 and 60 mg/L sodium arsenite (NaAsO 2) groups according to random number table method, six mice in each group. The pregnant mice were exposed to NaAsO 2 until weaning. After weaning, the offspring mice were still exposed to NaAsO 2 through drinking water till postnatal day (PND) 40. Morris water maze was used to determine the effects of arsenic exposure on learning and memory ability in PND 40 mice. The body weight of the mice was measured at PND 10, 20 or 40, and brain tissues were taken after the mice were sacrificed and the hippocampus was isolated. The levels of BDNF and TrkB mRNA in the hippocampus of offspring mice were measured by Real-time PCR. Results:There was significant difference in body weight of PND 20 offspring mice among the control, 15, 30 and 60 mg/L NaAsO 2 groups [(14.42 ± 1.88), (13.50 ± 1.38), (13.00 ± 1.14), (11.75 ± 0.82) g, F = 4.000, P < 0.05], the body weight of offspring mice in 60 mg/L NaAsO 2 group decreased significantly than that in control group( P < 0.05); there was significant difference in body weight of PND 40 offspring mice among groups [(38.58 ± 2.35), (37.17 ± 1.78), (35.67 ± 1.69), (33.83 ± 1.47) g, F = 7.248, P < 0.05], the body weights of offspring mice in 30 and 60 mg/L NaAsO 2 groups were significantly lower than that in control group, and the body weight of PND 40 offspring mice in 60 mg/L NaAsO 2 group was significantly lower than that in 15 mg/L NaAsO 2 group ( P < 0.05); the results of Morris water maze showed that there were significant differences in the escape latency of offspring mice among groups since 3 - 5 days of training ( F = 3.380, 6.788, 7.240, P < 0.05), the escape latency of offspring mice in NaAsO 2 groups [(67.76 ± 6.45), (71.47 ± 12.19), (73.96 ± 10.42), (58.63 ± 9.24), (60.20 ± 3.74), (67.96 ± 15.41) s] was significantly longer than that in control group [(52.83 ± 8.33), (43.39 ± 8.98) s] since 4 - 5 days of training ( P < 0.05); on the other hand, in the probe trail, there was significant difference in time spent in the target quadrant of offspring mice among groups ( F = 5.709, P < 0.05), time spent in the target quadrant of offspring mice in 30 and 60 mg/L NaAsO 2 groups [(18.85 ± 3.97), (16.90 ± 1.62) s] was significantly less than that in control group [(24.48 ± 3.18) s, P < 0.05]; there was significant difference in BDNF mRNA levels (1.00 ± 0.05, 0.98 ± 0.06, 0.85 ± 0.06, 0.68 ± 0.03) of PND 20 mice among groups ( F = 9.368, P < 0.05), BDNF mRNA level of mice exposed to 60 mg/L NaAsO 2 was significantly lower than that in control, 15 and 30 mg/L NaAsO 2 groups ( P < 0.05); there was significant difference in BDNF mRNA levels (1.00 ± 0.03, 0.75 ± 0.02, 0.76 ± 0.03, 0.73 ± 0.06) of PND 40 mice among groups ( F = 3.998, P < 0.05), and that of PND 40 mice exposed to NaAsO 2 decreased significantly than that in control group ( P < 0.05); there was significant difference in TrkB mRNA levels (1.00 ± 0.08, 0.71 ± 0.02, 0.73 ± 0.02, 0.68 ± 0.09) of PND 20 mice among groups ( F = 16.158, P < 0.05), and that of PND 20 mice exposed to NaAsO 2 were significantly lower than that in control group ( P < 0.05). Conclusion:Arsenic exposure could decrease the mRNA levels of BDNF and TrkB in the hippocampus of offspring mice, which may affect the ability of learning and memory.