Tengfei Liu,Jianguo Niu,Yuying Gao,Xuan Liu,Jianya Su
Flonicamid is an insecticide with a unique mode of action, primarily inhibiting the feeding behavior of sap-sucking insects. However, its molecular target remains controversial. Reports indicate that both flonicamid and pymetrozine affect insect behavior and mobility. To investigate further, we compared the susceptibility of three insect species ( Myzus persicae , Nilaparvata lugens , and Drosophila melanogaster ) to flonicamid and pymetrozine under two different feeding postures. Results showed that feeding posture did not affect the survival curves or mean lifespans of the three insects. However, insect lifespans were significantly reduced under exposure to either insecticide compared to untreated controls. The effects of the two insecticides on susceptibility and lifespan under different feeding postures were markedly different: feeding posture significantly influenced the sensitivity of aphids, planthoppers, and fruit flies to pymetrozine but had minimal effects on the sensitivity of aphids and planthoppers to flonicamid. Flonicamid had only a minor impact on fruit flies' sensitivity. Survival curve analysis also revealed significant differences under pymetrozine stress, while no such differences were observed under flonicamid stress. These findings indicate that flonicamid exerts different toxicological effects on target insects (aphids and planthoppers) versus non-target insects (fruit flies), depending on feeding posture. This suggests that the toxicological mechanisms of flonicamid differ substantially between target and non-target organisms, with implications that findings in non-target insects may not directly apply to target pests. Our study provides valuable insights and directions for further research into flonicamid's mode of action, aiding in elucidating its underlying mechanisms.
Mei Peng,Qiongli Su,Qing Zeng,Le Li,Zhihong Liu,Lei Xue,Yan Cheng,Yanjun Huang,Ting Tao,Hongwei Lv,Xiaohui Li,Xiaojun Tao,Peng Guo,Alex F. Chen,Xiaoping Yang
Anticancer potential of metformin has been extensively studied. However, its anticancer clinical use remains yet to be approved since sufficient concentration on target organs could not be achieved via conventional administration. To overcome this drawback, we aim to examine the efficiency of novel intravesical treatment of metformin on syngeneic orthotopic preclinical model. Three human and one murine bladder cancer cell lines were tested in vitro for inhibitory sensitivity by MTT and cologenic assays. AMPK pathway including AKT, Erk and S6K was examined by western blot and further explored by regulating activated levels using specific inhibitors. In vivo efficacy was determined by Kaplan-Meier survival curves and measurements of body and bladder weights plus tumor biomarkers. Lactic acid and metformin levels of plasma were measured by standard procedures. The results demonstrated that metformin activated AMPK and decreased phosphorylation of Akt and Erk. Furthermore, combinations of metformin with either Akt or Erk inhibitors synergistically diminished cancer proliferation, suggesting the involvement of Akt- and Erk- related pathways. Intravesical metformin 26 and 104 mg/kg, twice per week demonstrated a rapid elimination of the implanted tumor without any evidence of toxicity. In contrast, oral treatment at a dose of 800mg/kg/d exhibited little efficacy whereas severe toxicity existed if the dosage is higher. Collectively, intravesical metformin displays potent inhibition on bladder cancer in vitro and this preclinical study reveals the profound therapeutic application of metformin with durable tolerance via intravesical administration route.
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