Background Non-small cell lung cancers (NSCLC) account for most cases of lung cancer. More effort is needed to research new drug and combination therapies for this disease. An anthraquinone derivative, emodin shows anticancer potency. We hypothesis that emodin suppresses lung cancer cells through hyaluronan (HA) synthase 2-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway mediated cell cycle regulation. Methods We tested the effect of emodin on viability, apoptosis, and HA secretion of 5 NSCLC cell lines. We used NSCLC cells A549 for two rounds of knockdown study: (1) knocking down either the synthases (HAS2 and HAS3) or the receptors (CD44 and RHAMM); (2) knocking down either HAS2 or HAS3. Then determined the effect of emodin on viability, HA secretion, cell cycle, and expression of cyclin proteins. Results Emodin suppressed viability and HA secretion of all 5 NSCLC cell lines except for HA secretion of H460. Emodin had a slight apoptosis induction effect on all cell lines and was not different among cell lines. The knockdown of either the synthases or the receptors blocked emodin effects on viability while the knockdown of HAS2 block emodin effects but not HAS3. Emodin increased cells in the G1/G0 phase, and decreased cells in the S and G2/M phase by down-regulating cyclin A and B and up-regulating cyclin C, D, and E. HAS2 knockdown blocked the effects of emodin on the cell cycle. Conclusions This study demonstrated that emodin regulates the cell cycle of NSCLC cells through the HAS2-HA-CD44/RHAMM interaction-dependent signaling pathway.
Objective: This study explored the effects and mechanisms of Huangqi Guizhi Wuwu Decoction on chemotherapy-induced neuropathic pain (CINP). Methods: Bodyweight and related behavioral testing of the rat model were utilized to investigate the effects of Huangqi Guizhi Wuwu Decoction on CINP. ELISA was used to measure the levels of TNF-α, IL-1β, and IL-6, in the serum of chronic CINP rats. Immunohistochemistry and Western blot analysis were performed to detect the expression of MAPK pathway related-proteins namely ERK1/2, p38, and JNK, and the expression of downstream essential proteins such as c-Fos, CREB, and NF-κB. Results: Body weight and related behavioral testing of the rat model suggests that Huangqi Guizhi Wuwu Decoction can improve the slow weight gain of oxaliplatin-induced chronic CINP model rats and effectively prevent and treat oxaliplatin-induced regular CIPN rat model of hyperalgesia. It can also oppress the mechanical pain threshold, cold pain threshold, and heat pain threshold decreased. Furthermore, by ELISA, immunohistochemistry, and western blot analysis, we found that Huangqi Guizhi Wuwu Decoction can downregulate the levels of TNF-α, IL-1β, and IL-6 in the serum of chronic CINP rats induced by oxaliplatin. It also suppresses the expression of MAPK pathway related-proteins ERK1/2, p38, and JNK. This results in a decrease in the expression of downstream essential proteins, c-Fos, CREB, and Nf-κB. Conclusions: In conclusion, we found that Huangqi Guizhi Wuwu Decoction can combat nerve cell injury, reduce pain sensitization, and prevent and repair the damage of nerve cells in the oxaliplatin CINP model rats via TNFα/IL-1β/IL-6/MAPK/NF-kB pathway.
Background: The mechanism of Huangqi Guizhi Wuwu Decoction in the prevention and treatment of oxaliplatin-induced neuropathic pain was unclear. Therefore, we explored the effect and mechanism of Huangqi Guizhi Wuwu Decoction in chemotherapy-induced neuropathic pain (CINP). Methods: Bodyweight and related behavioral testing of the rat model were utilized to explore the effect of Huangqi Guizhi Wuwu Decoction in CINP. ELISA was used to detect the levels of TNF-α, IL-1β, IL-6 inflammatory factors in the serum of chronic CINP rats induced by oxaliplatin. Immunohistochemistry and western blot analysis were applied to detect the expression of MAPK pathway related-proteins ERK1/2, p38, JNK, and the expression of downstream essential proteins c-Fos, CREB, and NF-κB. Results: By bodyweight and related behavioral testing of the rat model, we found that Huangqi Guizhi Wuwu Decoction can improve the slow weight gain of oxaliplatin-induced chronic CINP model rats, effectively prevent and treat oxaliplatin-induced regular CIPN rat model of hyperalgesia, and oppress the mechanical pain threshold, cold pain threshold, and heat pain threshold decreased. By ELISA, immunohistochemistry, and western blot analysis, we found that Huangqi Guizhi Wuwu Decoction can down-regulate the levels of TNF-α, IL-1β, IL-6 inflammatory factors in the serum of chronic CINP rats induced by oxaliplatin, then suppressed the expression of MAPK pathway related-proteins ERK1/2, p38 and JNK. After that, the expression of downstream essential proteins c-Fos, CREB, and Nf-κB also decreased. Conclusion: In conclusion, we found that Huangqi Guizhi Wuwu Decoction can combat nerve cell injury, reduce pain sensitization, and prevent and repair the damage of nerve cells in oxaliplatin CINP model rats by TNFα/IL-1β/IL-6/MAPK/NF-kB pathway.
Review question / Objective: Myosteatosis may a better predictor than sarcopenia. Clinicians should strengthen the screening of myosteatosis in patients of GC and give active l support to improve the prognosis of patients. Eligibility criteria: We assigned two authors independently to search for relevant studies and screen the literature using titles and abstracts. After the initial screening, the full text of the articles that satisfied the inclusion criteria were evaluated. In this study, we established following inclusion criteria: 1) adults diagnosed with GC. 2) The primary outcome for these studies include overall survival (OS) or/and disease free survival (DFS) with myosteatosis or radiodensity as one of the variables. 3) The decrease of HU was used as the diagnostic criterion for myosteatosis. The exclusion criteria were as follows: 1) case reports, reviews, conference abstracts or preclinical studies, 2) studies citing literature with incomplete data, and 3) nonhuman studies. If the same patient cohort was used in multiple studies, the latest and more complete data were adopted in this meta-analysis. INPLASY registration number:This protocol was registered with the International Platform of Registered Systematic Review and Meta-Analysis Protocols (INPLASY) on 07 June 2023 and was last u p d a t e d o n 0 7 J u n e 2 0 2 3 ( r e g i s t r a t i o n n u m b e r INPLASY202360024).
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