Tubeimoside I

29434745

In the present study, the effects of tubeimoside I (TBMS1) on particulate matter <2.5 µm in diameter (PM2.5)-induced pulmonary injury and its mechanisms of action were investigated. Male BALB/c mice were randomly assigned into five groups (n=10/group): Control, PM2.5, PM2.5 + TBMS1 45 mg/kg, PM2.5 + TBMS1 90 mg/kg and PM2.5 + TBMS1 180 mg/kg. The dose of the PM2.5 suspension administered to the mice was 40 mg/kg via nasal instillation. The PM2.5 + TBMS1 groups received TBMS1 daily orally for 21 consecutive days, while the mice in the control and PM2.5 groups received equivalent volumes of PBS. Subsequently, lactic dehydrogenase, acid phosphatase, alkaline phosphatase, albumin, tumor necrosis factor-α and interleukin-6 protein levels in bronchoalveolar lavage fluid were determined. Oxidative stress was evaluated by detecting the protein levels of malondialdehyde, superoxide dismutase and inducible nitric oxide synthase, and the level of nitric oxide in lung tissue. Lastly, histopathological images of lung sections were obtained to observe changes in the lung tissue with treatment. The results indicated that exposure to PM2.5 induced pathological pulmonary changes, and biofilm and parenchymal cell damage, and promoted inflammation and oxidative stress. Treatment with TBMS1 attenuated the development of PM2.5-induced pulmonary injury. Its mechanisms of action were associated with reducing cytotoxic effects, levels of inflammatory mediators and oxidative damage. In conclusion, the results of the present study indicate that TBMS1 is a potential therapeutic drug for treating PM2.5-induced pulmonary injury.

inflammation; oxidative damage; particle matter <2.5 µm in diameter; pulmonary injury; tubeimoside I.

Tubeimoside I Attenuates Inflammation and Oxidative Damage in a Mice Model of PM 2.5-induced Pulmonary Injury

Jin-Bo Zhang 1 , Lei Zhang 2 , Shi-Qing Li 3 , Ai-Hua Hou 4 , Wei-Chao Liu 1 , Ling-Ling Dai 4

2018 Feb

30389907

Cervical cancer is one of the most aggressive human cancers with poor prognosis due to constant chemoresistance and repeated relapse. Tubeimoside I (TBM) has been identified as a potent antitumor agent that inhibits cancer cell proliferation by triggering apoptosis and inducing cell cycle arrest. Nevertheless, the detailed mechanism remains unclear and needs to be further elucidated, especially in cervical cancer. In this study, we found that TBM could induce proliferation inhibition and cell death in cervical cancer cells both in vitro and in vivo. Further results demonstrated that treatment with TBM could induce autophagosome accumulation, which was important to TBM against cervical cancer cells. Mechanism studies showed that TBM increased autophagosome by two pathways: First, TBM could initiate autophagy by activating AMPK that would lead to stabilization of the Beclin1-Vps34 complex via dissociating Bcl-2 from Beclin1; Second, TBM could impair lysosomal cathepsin activity and block autophagic flux, leading to accumulation of impaired autophagolysosomes. In line with this, inhibition of autophagy initiation attenuated TBM-induced cell death, whereas autophagic flux inhibition could exacerbated the cytotoxic activity of TBM in cervical cancer cells. Strikingly, as a novel lethal impaired autophagolysosome inducer, TBM might enhance the therapeutic effects of chemotherapeutic drugs towards cervical cancer, such as cisplatin and paclitaxel. Together, our study provides new insights into the molecular mechanisms of TBM in the antitumor therapy, and establishes potential applications of TBM for cervical cancer treatment in clinic.

Tubeimoside I Induces Accumulation of Impaired Autophagolysosome Against Cervical Cancer Cells by Both Initiating Autophagy and Inhibiting Lysosomal Function

Xuping Feng 1 2 , Jing Zhou 2 , Jingyi Li 3 , Xueyan Hou 4 , Longhao Li 1 5 , Yongmin Chen 6 , Shuyue Fu 2 , Li Zhou 2 , Changlong Li 7 , Yunlong Lei 8

2018 Nov 2