Materials and Methods: The study was conducted from 2018 to 2020 at a tertiary care teaching hospital. A total of 86 patients were treated with NPWT and their results were assessed for various parameters like reduction in wound size, discharge, infection, etc. We included patients with acute traumatic wounds as well as chronic infected wounds, and placed them in three treatment groups to receive either conventional NPWT, Indigenous NPWT and lastly NPWT with supplement TPOT.
Results: We observed a significant reduction of wound size, discharge and infection control in all three groups. The efficacy of indigenous NPWT is at par with conventional NPWT. Only six patients who had several comorbidities required flap coverage while in another four patients we could not achieve desired result due to technical limitations.
Conclusion: Indigenous NPWT with added TPOT is a very potent and cost effective method to control infection and rapid management of severe trauma seen in orthopaedic practice. It also decreases the dependency on plastic surgeons for management of such wounds.
Objective: In this study, we aimed to examine the effect of MAN on human lung cancer and reveal the underlying molecular mechanism.
Methods: MTT assay was conducted to measure cell viability. Annexin V-FITC/PI staining was used to detect cell apoptosis. Confocal microscope was performed to determine the formation of autophagosomes and autolysosomes. Flow cytometry was performed to quantify cell death. Western blotting was used to determine the related-signaling pathway.
Results: In the present study, we demonstrated for the first time that MAN inhibitd cell proliferation and induced cell apoptosis in human non-small-cell lung carcinoma (NSCLC) cells. We found that MAN treatment dysregulated mitochondrial function and led to mitochondrial apoptosis in A549 and PC9 cells. Meanwhile, MAN enhanced autophagy flux by the increase of autophagosome formation, the fusion of autophagsomes and lysosomes and lysosomal function. Moreover, mTOR signaling pathway, a classical pathway regualting autophagy, was inhibited by MAN in a time- and dose-dependent mannner, resulting in autophagy induction. Interestingly, autophagy inhibition by CQ or Atg5 knockdown attenuated cell apoptosis by MAN, indicating that autophagy serves as cell death. Furthermore, autophagy-mediated cell death by MAN can be blocked by reactive oxygen species (ROS) scavenger NAC, indicating that ROS accumulation is the inducing factor of apoptosis and autophagy. In summary, we revealed the molecular mechanism of MAN against lung cancer through apoptosis and autophagy, suggesting that MAN might be a novel therapeutic agent for NSCLC treatment.