Bajitianwan attenuates D-galactose-induced memory impairment and bone loss through suppression of oxidative stress in aging rat model

2020 ◽  
Vol 261 ◽  
pp. 112992
Author(s):  
Wumu Xu ◽  
Xiaoyan Liu ◽  
Xuhui He ◽  
Yiping Jiang ◽  
Jiabao Zhang ◽  
...  
2017 ◽  
Vol 8 ◽  
Author(s):  
Alrieta H. Teixeira ◽  
Jordânia M. de Oliveira Freire ◽  
Luzia H. T. de Sousa ◽  
Antônia T. Parente ◽  
Nayara A. de Sousa ◽  
...  

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Gaurav Patki ◽  
Farida Allam ◽  
Ritu Bohat ◽  
Faizan Jafri ◽  
Mohammad Saleem ◽  
...  

2020 ◽  
Vol 35 (6) ◽  
pp. 569-578
Author(s):  
Chun Yao ◽  
Qingqing Zhang ◽  
Jun Li ◽  
Peng She ◽  
Fanzhi Kong ◽  
...  

The effect of implantable Zoledronate-PLGA microcapsules (PLGA-ZOL) in periodontitis remains unclear. In this study, we aimed to explore the potential role of PLGA-ZOL in protecting periodontitis and elucidate the underlying mechanism. A rat model of periodontitis was established by ligation the mandibular first molars, then PLGA-ZOL was implanted. The healing volume was scanned by cone-beam computed tomography. Cytokine levels in the gingival tissues were determined by ELISA and RT-PCR. Oxidative stress was indicated by detecting superoxide dismutase concentration and catalase activity. After periodontitis model was successfully established in rats, PLGA-ZOL treatment significantly attenuated alveolar bone loss, as indicated by the increased total healing volume, bone volume/tissue volume and osteoprotegerin level, as well as decreased sRANKL level. PLGA-ZOL treatment also suppressed the inflammatory activities by inhibiting pro-inflammatory cytokine production (TNF-α, IL-1β) but increasing anti-inflammatory cytokine secretion (IL-10). Furthermore, PLGA-ZOL was found to ameliorate oxidative stress in gingival tissues. In conclusion, PLGA-ZOL microcapsules ameliorate alveolar bone loss, gingival inflammation and oxidative stress in an experimental rat model of periodontitis.


PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183506 ◽  
Author(s):  
Aurigena Antunes de Araújo ◽  
Aline de Sousa Barbosa Freitas Pereira ◽  
Caroline Addison Carvalho Xavier de Medeiros ◽  
Gerly Anne de Castro Brito ◽  
Renata Ferreira de Carvalho Leitão ◽  
...  
Keyword(s):  

Author(s):  
Karem H. Alzoubi ◽  
Arwa M. Al-Dekah ◽  
Saied Jaradat ◽  
Nasr Alrabadi

Background: Post-traumatic stress disorder (PTSD) is a genuine obstructing mental disorder. As indicated by the name, it is related to the patients’ stress augmented by life-threatening conditions or accidents. The PTSD has linked to oxidative stress that can result in neurodegeneration. L-carnitine (L-CAR) is known for its antioxidant properties, which can protect against neuronal damage. Objective: In the current study, we investigated the beneficial effects of L-CAR on the memory impairment induced by PTSD using a rat model. Methods: A model of single-prolonged stress (a cycle of restraining, forced swimming, rest, and finally diethyl ether exposure for 2 h, 20 min, 15 min, and 1–2 min, respectively) was used to induce PTSD-like behavior. Intraperitoneal L-CAR treatment (300 mg/kg/day) was introduced for four weeks. Both memory and special learning were evaluated utilizing the radial arm water maze (RAWM). Moreover, the levels of glutathione peroxidase (GPx), glutathione reduced (GSH), and glutathione oxidized (GSSG) were assessed as biomarkers oxidative stress in the hippocampus. Results: The results demonstrated that both the short and long-term memories were impaired by PTSD/SPS model (P <  0.05), while L-CAR treatment prevented this memory impairment in PTSD rats. Besides, L-CAR prevented the reduction in GPx activity and increase in GSSG, which were altered in the hippocampus of the PTSD/SPS rats (P <  0.05). Levels of GSH were not changed in PTSD and/or L-CAR rats. Conclusions: L-CAR administration prevented short- and long-term memories’ impairments induced in the PTSD/SPS rat model. This is probably related to its antioxidant effects in the hippocampus.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 93-93
Author(s):  
Hyoeun Yoo ◽  
Hyun-Sook Kim

Abstract Objectives Healthy aging is one of the most attentive topics since senescence may lead to retrogression of antioxidative ability, inflammatory regulation and neurodegeneration. This study was performed to determine the antioxidative effects of cacao powder supplementation in d-galactose induced aging rat model. Methods After 3 weeks of adaptation period, 12-week-old SD rats were randomly divided into four groups (n = 8 each): Control group (C), D-galactose induced aging group (G), D-galactose injection with 10% cacao powder group (LC), D-galactose injection with 16% cacao powder group (HC) (10%, 16% is % per total food weight). G, LC, HC groups were intraperitoneally injected with D-galactose for 8 weeks and C group was treated with saline as a substitute. Results After 8 weeks of cacao powder supplementation, serum malondialdehyde (MDA), advanced glycation end (AGE) levels, and Liver malondialdehyde (MDA) level significantly decreased in LC, HC group compared to G group (P &lt; 0.05). Protein expression of SOD2 and CAT in the brain showed significant increase in LC and HC group compared to G group (P &lt; 0.05). Protein expression of Gpx1 in the brain tends to increase in LC and HC group compared to G group but did not show statistical significance. Conclusions This study demonstrates that dietary cacao powder supplementation can alleviate oxidative stress by regulating oxidative stress markers like MDA and AGE or antioxidant enzymes such as SOD2 and CAT in d-galactose induced aging rat model. Funding Sources This study was funded by Nutritional Immunology Lab of Sookmyung Women's University.


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