Efficacy of some non-conventional herbal medications (sulforaphane, tanshinone IIA, and tetramethylpyrazine) in inducing neuroprotection in comparison with interleukin-10 after spinal cord injury: A meta-analysis

Koushki, Davood; Latifi, Sahar; Javidan, Abbas Norouzi; Matin, Marzieh

doi:10.1179/2045772314y.0000000215

Cited by 24 publications

(16 citation statements)

References 66 publications

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“…We also confirmed that tan IIA prevented streptozotocininduced memory deficits in mice [20]. Recently, our experimental data revealed that tan IIA inhibited endoplasmic reticulum stress-induced apoptosis in APPswe/ PS1dE9 (referred to as APP/PS1) transgenic mice and SH-SY5Y cells [24,25], although increasing evidence showed that tan IIA exhibits anti-inflammatory activity both in vivo and in vitro [21,[26][27][28]. However, the effects of tan IIA on RAGE-mediated neuroinflammation and its underlying molecular mechanisms in AD are not reported.…”

Section: Introductionsupporting

confidence: 78%

Tanshinone IIA attenuates neuroinflammation via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro

Ding

Lin

Liu

et al. 2020

J Neuroinflammation

114

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Background Glial activation and neuroinflammation play a crucial role in the pathogenesis and development of Alzheimer’s disease (AD). The receptor for advanced glycation end products (RAGE)-mediated signaling pathway is related to amyloid beta (Aβ)-induced neuroinflammation. This study aimed to investigate the neuroprotective effects of tanshinone IIA (tan IIA), a natural product isolated from traditional Chinese herbal Salvia miltiorrhiza Bunge, against Aβ-induced neuroinflammation, cognitive impairment, and neurotoxicity as well as the underlying mechanisms in vivo and in vitro. Methods Open-field test, Y-maze test, and Morris water maze test were conducted to assess the cognitive function in APP/PS1 mice. Immunohistochemistry, immunofluorescence, thioflavin S (Th-S) staining, enzyme-linked immunosorbent assay (ELISA), real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and western blotting were performed to explore Aβ deposition, synaptic and neuronal loss, microglial and astrocytic activation, RAGE-dependent signaling, and the production of pro-inflammatory cytokines in APP/PS1 mice and cultured BV2 and U87 cells. Results Tan IIA treatment prevented spatial learning and memory deficits in APP/PS1 mice. Additionally, tan IIA attenuated Aβ accumulation, synapse-associated proteins (Syn and PSD-95) and neuronal loss, as well as peri-plaque microgliosis and astrocytosis in the cortex and hippocampus of APP/PS1 mice. Furthermore, tan IIA significantly suppressed RAGE/nuclear factor-κB (NF-κB) signaling pathway and the production of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) in APP/PS1 mice and cultured BV2 and U87 cells. Conclusions Taken together, the present results indicated that tan IIA improves cognitive decline and neuroinflammation partly via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro. Thus, tan IIA might be a promising therapeutic drug for halting and preventing AD progression.

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Section: Introductionsupporting

confidence: 78%

Tanshinone IIA attenuates neuroinflammation via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro

Ding

Lin

Liu

et al. 2020

J Neuroinflammation

114

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“…Mounting evidence has shown that besides of the benefit of endogenous IL-10, exogenous IL-10 also had obvious neuroprotection and neuro-recovery properties in animal models; even more efficient than some anti-inflammatory and anti-oxidative agents [53]. Considering these data together with the findings from this study, IL-10 may be a potentially useful drug for the treatment of diabetic neuropathy.…”

Section: Discussionsupporting

confidence: 66%

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

Bao²,

Men

et al. 2019

Exp Clin Endocrinol Diabetes

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Demyelination resulting from Schwann cell injury is a main pathological feature of diabetic neuropathy, and a key contributor to this process may be inflammation due to advanced glycation end products (AGEs). Therefore, protection by anti-inflammation agents is anticipated. In this study, we showed that interleukin-10 (IL-10), an anti-inflammatory cytokine, inhibits apoptosis of Schwann cells induced by AGEs in vitro. We isolated and cultured Schwann cells from rat sciatic nerves. As detected by flow cytometry, apoptosis of Schwann cells markedly increased following incubation with AGEs for 48 h. However, pretreatment with IL-10 inhibited AGE-induced apoptosis. The effect of IL-10 on NF-κB, which is a very important regulator of inflammation, was also evaluated, and results showed high levels of phospho-NF-κB and nuclear localization of NF-κB in cells incubated with AGEs but low levels of phospho-NF-κB and cytoplasmic localization in the cells incubated with IL-10, indicating the activation of NF-κB by AGEs and inhibition of NF-κB by IL-10. Moreover, incubating Schwann cells with an NF-κB inhibitor (caffeic acid phenethyl ester) for 30 min before adding AGEs mimicked IL-10, lowering the amount of reactive oxygen species and activity of caspase-3 and also decreasing apoptosis in Schwann cells. These results indicate that IL-10 may protect Schwann cells against AGE-induced apoptosis by attenuating oxidative stress via the inhibition of activation of NF-κB.

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“…The results showcased the protective ability of PA in PC12 cells against H 2 O 2 -evoked impairment, which was presented as accelerating cell viability, repressing TCMs have been shown the effective functions in remedying SCI, especially S. miltiorrhiza [15,16]. The existing evidences attest that S. miltiorrhiza emerges a beneficial role in impeding secondary damage after acute SCI, which also can fight cell apoptosis and accelerate nerve repair [17,18]. A rat SCI model experiment disclosed that the extractions from S. miltiorrhiza could effectively relieve SCI [19].…”

Section: Discussionmentioning

confidence: 92%

Protocatechuic aldehyde mitigates hydrogen peroxide-triggered PC12 cell damage by down-regulating MEG3

Zhong

Yao

Luo

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Protocatechuic aldehyde (PA) extracts from S. miltiorrhiza, which anti-oxidative and antiinflammatory functions have been certified in diverse diseases. Nonetheless, the influence of PA in spinal cord injury (SCI) is still hazy. The research probed the function of PA in hydrogen peroxide (H 2 O 2)damaged PC12 cells. Methods: The disparate dosages of H 2 O 2 (0-400 mM) or PA (0-2 mM) were applied for stimulating PC12 cells, and subsequently cell viability, apoptosis, apoptosis-and autophagy-correlative factors were evaluated. After pc-MEG3 transfection, functions of MEG3 overexpression in H 2 O 2 and/or PA-managed PC12 cells were reassessed. Western blot was conducted to determine Wnt/b-catenin and PTEN/PI3K/ AKT pathways. Results: H 2 O 2 stimulation clearly triggered PC12 cell damage via prohibiting cell viability and accelerating apoptosis and autophagy. But, PA management mitigated H 2 O 2-triggered PC12 cells damage. Down-regulated MEG3 triggered by PA was presented in H 2 O 2-managed cells. What's more, overexpressed MEG3 dramatically overturned the influences of PA in H 2 O 2-damaged PC12 cells. Beyond that, PA activated Wnt/b-catenin and PTEN/PI3K/AKT via repression of MEG3 in H 2 O 2-managed PC12 cells. Conclusions: The results disclosed the protective impacts of PA on PC12 cells to resist H 2 O 2-provoked damage. MEG3, Wnt/b-catenin and PTEN/PI3K/AKT pathways joined in adjusting the activity of PA in H 2 O 2-damaged PC12 cells.

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Efficacy of some non-conventional herbal medications (sulforaphane, tanshinone IIA, and tetramethylpyrazine) in inducing neuroprotection in comparison with interleukin-10 after spinal cord injury: A meta-analysis

Cited by 24 publications

References 66 publications

Tanshinone IIA attenuates neuroinflammation via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro

Tanshinone IIA attenuates neuroinflammation via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

Protocatechuic aldehyde mitigates hydrogen peroxide-triggered PC12 cell damage by down-regulating MEG3

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