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        Ginsenoside Rg1 enhances the healing of injured tendon in achilles tendinitis through the activation of IGF1R signaling mediated by oestrogen receptor

        Tianyi Wu,Wenxiao Qi,Haojie Shan,Bin Tu,Shilin Jiang,Ye Lu,Feng Wang 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4

        Background: During the pathogenesis of tendinopathy, the chronic inflammation caused by the injury and apoptosis leads to the generation of scars. Ginsenoside Rg1 (Rg1) is extracted from ginseng and has anti-inflammatory effects. Rg1 is a unique phytoestrogen that can activate the estrogen response element. This research aimed to explore whether Rg1 can function in the process of tendon repair through the estrogen receptor. Methods: In this research, the effects of Rg1 were evaluated in tenocytes and in a rat model of Achilles tendinitis (AT). Protein levels were shown by western blotting. qRT-PCR was employed for evaluating mRNA levels. Cell proliferation was evaluated through EdU assay and cell migration was evaluated by transwell assay and scratch test assay. Results: Rg1 up-regulated the expression of matrix-related factors and function of tendon in AT rat model. Rg1 reduced early inflammatory response and apoptosis in the tendon tissue of AT rat model. Rg1 promoted tenocyte migration and proliferation. The effects of Rg1 on tenocytes were inhibited by ICI182780. Rg1 activates the insulin-like growth factor-I receptor (IGF1R) and MAPK signaling pathway. Conclusion: Rg1 promotes injured tendon healing in AT rat model through IGF1R and MAPK signaling pathway activation.

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        Protective effect of Lactobacillus plantarum ATCC8014 on acrylamide-induced oxidative damage in rats

        Zhao Sijia,Zhao Xiaoduo,Liu Qingbo,Jiang Yujun,Li Yanhua,Feng Wenxiao,Xu Honghua,Shao Meili 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.4

        Acrylamide (AA), which is mainly found in fried foods, causes neurotoxicity, genetic toxicity, carcinogenic effects, and DNA damage. This study confirms that a strain of lactic acid bacteria (Lactobacillus plantarum ATCC8014) could alleviate the toxicity of rats by inhibiting the AA-induced oxidative damage. Forty-eight adult male SD rats were randomly divided into eight groups: control group, AA group (40 mg/kg), three different doses (1 × 107 CFU/ml, 1 × 108 CFU/ ml, 1 × 109 CFU/ml of Lactobacillus plantarum ATCC8014) of prevention groups and therapeutic groups, respectively. At the end of three-week experiment, AA treatment produced a significant reduction in the rate of weight gain along with the symptoms of hind limb splay and ataxia. Histological examinations revealed various degrees of injury in five tissues. Levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in group AA rats were significantly decreased, but the level of lipid peroxidation (LPO) was significantly increased (p < 0.05). Both prevention and therapeutic groups with 1 × 109 CFU/ml of Lactobacillus plantarum ATCC8014 could effectively reduce the injury of AA to the body. However, reductions in both groups were not statistically significant.

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