Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Hao, Jian; Wang, Ping; Daiping, Pei; Jia, Bin; Qun-sheng, HU

doi:10.1002/kjm2.12123

Cited by 6 publications

(2 citation statements)

References 39 publications

(94 reference statements)

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“…According to previous research, rhein can sensitize human pancreatic cancer cells to EGFR inhibitors by inhibiting the STAT3 pathway (Yang et al, 2019). In addition, Hao et al found that rhein improved motor function in rats with spinal cord injury by inhibiting the P38/MAPK pathway (Hao et al, 2019). Ma et al showed that rhein can affect the malignant phenotype of renal cancer by inhibiting MAPK/NF-κB signaling (Ma et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways

Zhang

et al. 2022

Front. Pharmacol.

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The progression from compensatory hypertrophy to heart failure is difficult to reverse, in part due to extracellular matrix fibrosis and continuous activation of abnormal signaling pathways. Although the anthraquinone rhein has been examined for its many biological properties, it is not clear whether it has therapeutic value in the treatment of cardiac hypertrophy and heart failure. In this study, we report for the first time that rhein can ameliorate transverse aortic constriction (TAC)-induced cardiac hypertrophy and other cardiac damage in vivo and in vitro. In addition, rhein can reduce cardiac hypertrophy by attenuating atrial natriuretic peptide, brain natriuretic peptide, and β-MHC expression; cardiac fibrosis; and ERK phosphorylation and transport into the nucleus. Furthermore, the inhibitory effect of rhein on myocardial hypertrophy was similar to that of specific inhibitors of STAT3 and ERK signaling. In addition, rhein at therapeutic doses had no significant adverse effects or toxicity on liver and kidney function. We conclude that rhein reduces TAC-induced cardiac hypertrophy via targeted inhibition of the molecular function of ERK and downregulates STAT3 and p38 MAPK signaling. Therefore, rhein might be a novel and effective agent for treating cardiac hypertrophy and other cardiovascular diseases.

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Section: Discussionmentioning

confidence: 99%

Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways

Zhang

et al. 2022

Front. Pharmacol.

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“…3.8. Mt activates the MAPK signaling pathway in vitro and in vivo JNK, Erk1/2, and p38 MAPK, three important members of mitogen-activated protein kinase (MAPK) family, are closely associated with apoptosis and oxidative stress [33,34]. To determine whether Mt triggers MAPK signaling, the expression and phosphorylation of MAPK signaling proteins was respectively detected by Western blot and immuno uorescence staining, both in vitro and in vivo.…”

Section: Nac Pretreatment Attenuated Mt-induced Cytotoxicitymentioning

confidence: 99%

ROS generation and p-38 activation contribute to montmorillonite-induced corneal toxicity in vitro and in vivo

Liu

Yang

Zhao

et al. 2022

Preprint

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Background Montmorillonite (Mt) and its derivatives are now widely used in industrial and biomedical fields. Therefore, safety assessments of these materials are critical to protect human health after exposure; however, studies on the ocular toxicity of Mt are lacking. In particular, varying physicochemical characteristics of Mt may greatly alter their toxicological potential. To explore the effects of such characteristics on the eyes, five types of Mt were investigated in vitro and in vivo for the first time, and their underlying mechanisms studied. Results The different types of Mt caused cytotoxicity in human HCEC-B4G12 corneal cells based on analyses of ATP content, lactate dehydrogenase leakage, cell morphology, and the distribution of Mt in cells. Among the five Mt types, Na-Mt exhibited the highest cytotoxicity. Notably, Na-Mt and chitosan-modified acidic Na-Mt (C-H-Na-Mt) induced ocular toxicity in vivo, as demonstrated by increases corneal injury area and the number of apoptotic cells. Na-Mt and C-H-Na-Mt also induced reactive oxygen species (ROS) generation in vitro and in vivo, as indicated by 2′,7′-dichlorofluorescin diacetate and dihydroethidium staining. In addition, Na-Mt activated the mitogen-activated protein kinase signaling pathway. The pretreatment of HCEC-B4G12 cells with N-acetylcysteine, an ROS scavenger, attenuated the Na-Mt-induced cytotoxicity and suppressed p38 activation, while inhibiting p38 activation with a p38-specific inhibitor decreased Na-Mt-induced cytotoxicity. Conclusions The results indicate that Mt induces corneal toxicity in vitro and in vivo. The physicochemical properties of Mt greatly affect its toxicological potential. Furthermore, ROS generation and p38 activation contribute at least in part to Na-Mt-induced toxicity.

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Recent advances on signaling pathways and their inhibitors in spinal cord injury

Ding,

Chen

2024

Biomedicine & Pharmacotherapy

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Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Cited by 6 publications

References 39 publications

Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways

Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways

ROS generation and p-38 activation contribute to montmorillonite-induced corneal toxicity in vitro and in vivo

Recent advances on signaling pathways and their inhibitors in spinal cord injury

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