Pro‑neurogenic effects of andrographolide on RSC96 Schwann cells in vitro
Authors: Peizhen Lv
Fuben Xu
Kun Zhang
Huayu Wu
Jinmin Zhao
Li Zheng
Journal: Molecular Medicine Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: Nerve regeneration; Andrographolide; Schwann cells; Peripheral nerve injury; Anti-inflammatory agent
Affiliations: Research Center for Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China., Department of Cell Biology and Genetics, School of Premedical Sciences, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

Abstract:  Nerve regeneration remains a challenge to the treatment of peripheral nerve injury. Andrographolide (Andro) is the main active constituent of Andrographis paniculata, which has been applied in the treatment of several diseases, including inflammation, in ancient China. Andro has been reported to facilitate the reduction of edema and to exert analgesic effects in the treatment of various diseases. These findings suggest that Andro may be considered a promising anti‑inflammatory agent that may suppress destruction and accelerate proliferation of Schwann cells following peripheral nerve injury. In the present study, the effects of Andro on RSC96 cells were investigated in vitro. The RSC96 cell line is a spontaneously immortalized rat Schwann cell line, which was originally derived from a long‑term culture of rat primary Schwann cells. RSC96 cells were treated with a range of 0 to 50 µM Andro prior to the MTT assay. Cell proliferation, morphology, synthesis and nerve‑specific gene expression were performed to detect the effect of Andro on RSC96 cells. The results of the present study demonstrated that the recommended doses of Andro ranged between 0.78 and 12.5 µM, among which the most obvious response was observed when used at 3.125 µM (P&lt;0.05). DNA content was improved in Andro groups compared with the control group (P&lt;0.05). In addition, Andro was able to promote the gene expression of glial cell line‑derived neurotrophic factor, brain‑derived neurotrophic factor, ciliary neurotrophic factor, and the specific Schwann cell marker S100β (P&lt;0.05). The results of a viability assay, hematoxylin‑eosin staining, and immunohistochemistry were also improved in Andro groups. These results indicated that Andro may accelerate proliferation of RSC96 cells in vitro, whilst maintaining the Schwann cell phenotype; therefore, the present study may provide valuable evidence for the further exploration of the effects of Andro on peripheral nerves. 

Retracted: No

PubPeer comments:
 Figure 4 apparently includes 2 overlapping images representing different treatments. See green boxes below. *** ![file] , 
 [Corrigendum] Prou2011neurogenic effects of andrographolide on RSC96 Schwann cells in vitro Fuben Xu et al. Mol Med Rep. 2020 Sep. Abstract Following the publication of the above article, an interested reader drew to the authors attention that a pair of the data panels shown in Fig. 4 contained overlapping data. After having consulted their original data, the authors realized that a total of three panels featured in Figs. 4 and 6 had been erroneously selected. The image of hematoxylin and eosin (H E) staining for RSC96 Schwann cells in the 1.5625 u00b5M andrographolide for 6 days data panel in Fig. 4 (bottom row, second panel from the left) was mistakenly submitted. In addition, in Fig. 6, the images of immunohistochemical staining for RSC96 Schwann cells in the 3.125 u00b5M for 4 days panel (middle row, second panel from the right) and the 6.25 u00b5M for 6 days panel (bottom row, furthest panel on the right) were mistakenly submitted. The corrected versions of Figs. 4 and 6 are shown opposite. These corrections were approved by all authors. The authors regret that these errors were featured in the paper, even though they did not substantially alter any of the major conclusions reported in the study. Morever, the authors apologize to the Editor of Molecular Medicine Reports and to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 14: 3573u20113580, 2016; DOI: 10.3892 mmr.2016.5717]. *** ![file] ![file] ,