Molecular Mechanism of Extractum Liquidum Drug Loading Materials on Promoting Chronic Wound Tissue Repair Through Phosphatidylinositol 3 Kinase/Protein Kinase B/Hypoxia Induction Factor 1α Signal Pathway

2022 ◽  
Vol 12 (1) ◽  
pp. 52-60
Author(s):  
Hui Ji ◽  
Qian Zhang ◽  
Zengmin Yang ◽  
Minjie Rui ◽  
Qiyi Chen ◽  
...  
Keyword(s):  
Wound Healing ◽  
Protein Kinase ◽  
Molecular Mechanism ◽  
Healing Rate ◽  
Chronic Wound ◽  
Protein Kinase B ◽  
Signal Molecules ◽  
Group Model ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

To solve the shortcomings of traditional Zeji extractum liquidum (traditional Chinese medicine used for wound healing), and to explore the effect of Zeji Etractum Lquidum (ZLE) Nano Materials (ZLENM) on chronic wound (CW) healing and its molecular mechanism. 30 SD rats were divided into 3 groups in random: control group (Ctrl group), model group (CW group), and treatment group (ZLENM group). The results of wound healing rate showed that, in contrast with the CW, the healing rate of back wounds in the ZLENM group was greatly increased on the 7th and 14th days (P < 0.05). In contrast with the Ctrl, the rats in the CW and the ZLENM groups had greatly increased CD31 positive staining on the 7th and 14th days (P < 0.05), and the CW was lower than the ZLENM group (P < 0.05). In contrast with the 7th day, the MVD in the CW and the ZLENM groups was greatly reduced on the 14th day (P < 0.05). Western blot analysis of the expression of related signal molecules showed that the expressions of P-Akt, P-PI3K, HIF-1α, and VEGFR2 protein in the wounds in the CW and ZLENM groups were greatly increased in contrast with the Ctrl (P < 0.05), and CW was lower than ZLENM group (P < 0.05). In conclusion, ZLENM can promote wound healing and increase the number of wound angiogenesis in CW rats. The mechanism is related to the activation of phosphatidylinositol 3 kinase/protein kinase B/hypoxia induction factor 1α (PI3K/AKT/HIF-1α) signaling pathway.

scholarly journals Insulin Accelerates Inter-endosomal GLUT4 Traffic via Phosphatidylinositol 3-Kinase and Protein Kinase B

2001 ◽  
Vol 276 (47) ◽  
pp. 44212-44221 ◽  
Author(s):  
Leonard J. Foster ◽  
Dailin Li ◽  
Varinder K. Randhawa ◽  
Amira Klip
Keyword(s):  
Protein Kinase ◽  
Protein Kinase B ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

Expression of a prenylation-deficient Rab4 inhibits the GLUT4 translocation induced by active phosphatidylinositol 3-kinase and protein kinase B

2001 ◽  
Vol 356 (1) ◽  
pp. 143-149 ◽  
Author(s):  
Mireille CORMONT ◽  
Nadine GAUTIER ◽  
Karine ILC ◽  
Yannick Le MARCHAND-BRUSTEL
Keyword(s):  
Protein Kinase ◽  
Protein Kinase B ◽  
Active Form ◽  
Small Gtpase ◽  
Dominant Negative ◽  
Glut4 Translocation ◽  
Phosphatidylinositol 3 Kinase ◽  
Isolated Adipocytes ◽  
Phosphatidylinositol 3

The small GTPase Rab4 has been shown to participate in the subcellular distribution of GLUT4 under both basal and insulin-stimulated conditions in adipocytes. In the present work, we have characterized the effect of Rab4 ΔCT, a prenylation-deficient and thus cytosolic form of Rab4, in this process. We show that the expression of Rab4 ΔCT in freshly isolated adipocytes inhibits insulin-induced GLUT4 translocation, but only when this protein is in its GTP-bound active form. Further, it not only blocks the effect of insulin, but also that of a hyperosmotic shock, but does not interfere with the effect of zinc ions on GLUT4 translocation. Rab4 ΔCT was then shown to prevent GLUT4 translocation induced by the expression of an active form of phosphatidylinositol 3-kinase or of protein kinase B, without altering the activities of the enzymes. Our results are consistent with a role of Rab4 ΔCT acting as a dominant negative protein towards Rab4, possibly by binding to Rab4 effectors.

scholarly journals Vitamin D3 Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Yanyan He ◽  
Yang Liu ◽  
Qing-Zhu Wang ◽  
Feng Guo ◽  
Fengjuan Huang ◽  
...  
Keyword(s):  
Vitamin D ◽  
Growth Factor ◽  
Protein Kinase ◽  
Protein Kinase B ◽  
Diabetic Rats ◽  
Testicular Function ◽  
Insulin Like Growth Factor ◽  
Wild Type ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

Objective. In diabetes mellitus, vitamin D3 deficiency affects sex hormone levels and male fertility; however, the mechanism leading to the disorder is unclear. This research was designed to investigate the mechanism of vitamin D3 deficiency and hypogonadism in diabetic rats. Our aim was to assess serum vitamin D3 levels and the relationship among vitamin D3, insulin-like growth factor-1 (IGF-1), and testicular function. Materials and Methods. Rats with streptozotocin-induced diabetes were randomly divided into four groups and treated with different doses of vitamin D3: no vitamin D3, low (0.025 μg/kg/day), high (0.1 μg/kg/day), and high (0.1 μg/kg/day) with JB-1 (the insulin-like growth factor-1 receptor inhibitor group, 100 μg/kg/day). The groups were compared with wild-type rats, which function as the control group. Various parameters such as vitamin D3 and IGF-1 were compared between the experimental and wild-type groups, and their correlations were determined. Results. Twelve weeks of vitamin D3 supplementation improved the testosterone levels, as shown by the increase in the level of serum IGF-1 in diabetic rats. Phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT), which was a downstream of the signaling pathway of IGF-1, was significantly increased after vitamin D3 treatment. Conclusions. The study shows that vitamin D3 may promote the expression of testosterone and improve testicular function in diabetic rats by activating PI3K/AKT via IGF-1.

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