1.Dimethyl fumarate modulates M1/M2 macrophage polarization to ameliorate periodontal destruction by increasing TUFM-mediated mitophagy.
Liang CHEN ; Pengxiao HU ; Xinhua HONG ; Bin LI ; Yifan PING ; ShuoMin CHEN ; Tianle JIANG ; Haofu JIANG ; Yixin MAO ; Yang CHEN ; Zhongchen SONG ; Zhou YE ; Xiaoyu SUN ; Shufan ZHAO ; Shengbin HUANG
International Journal of Oral Science 2025;17(1):32-32
Periodontitis is a common oral disease characterized by progressive alveolar bone resorption and inflammation of the periodontal tissues. Dimethyl fumarate (DMF) has been used in the treatment of various immune-inflammatory diseases due to its excellent anti-inflammatory and antioxidant functions. Here, we investigated for the first time the therapeutic effect of DMF on periodontitis. In vivo studies showed that DMF significantly inhibited periodontal destruction, enhanced mitophagy, and decreased the M1/M2 macrophage ratio. In vitro studies showed that DMF inhibited macrophage polarization toward M1 macrophages and promoted polarization toward M2 macrophages, with improved mitochondrial function, inhibited oxidative stress, and increased mitophagy in RAW 264.7 cells. Furthermore, DMF increased intracellular mitochondrial Tu translation elongation factor (TUFM) levels to maintain mitochondrial homeostasis, promoted mitophagy, and modulated macrophage polarization, whereas TUFM knockdown decreased the protective effect of DMF. Finally, mechanistic studies showed that DMF increased intracellular TUFM levels by protecting TUFM from degradation via the ubiquitin-proteasomal degradation pathway. Our results demonstrate for the first time that DMF protects mitochondrial function and inhibits oxidative stress through TUFM-mediated mitophagy in macrophages, resulting in a shift in the balance of macrophage polarization, thereby attenuating periodontitis. Importantly, this study provides new insights into the prevention of periodontitis.
Dimethyl Fumarate/pharmacology*
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Mitophagy/drug effects*
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Animals
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Mice
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Macrophages/metabolism*
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Periodontitis/prevention & control*
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RAW 264.7 Cells
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Oxidative Stress/drug effects*
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Peptide Elongation Factor Tu/metabolism*
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Mice, Inbred C57BL
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Male
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Mitochondria/drug effects*
2.Relationship of k-ras mutation and colorectal cancer
Huijuan CHEN ; Hongbo LI ; Shuomin LI ; Biwen LU ; Junfeng CHENG ; Yuanli LIU
Cancer Research and Clinic 2010;22(7):461-463
Objective To explore the status of mutations of k-ras gene in colorectal cancer (CRC) patients and to make theory preparation for the k-ras mutation detection in diagnosis laboratory. Methods The Genomic DNA was extracted, mutation analysis of k-ras was detected by PCR and bi-direction sequencing in the 56 specimens. Results Rate of k-ras mutation was 46.63 % (26/56) including 76.92 % (20/26) located at codon 12, and 23.08 %(6/26) located at codon 13, and no mutation was found at both codons simultaneously. G>A transition is the most common type of k-ras mutation,GGT>GAT (G12D) is the predominant mutation at codon 12 and GGOGAC (G13D) at codonl3. Chi-square analysis revealed the k-ras mutation was significantly correlated to the gender of the patients. Conclusion The k-ras mutation is mainly located at the codon 12, G>A transition is the most type of k-ras mutation in CRC. k-ras mutation seems to correlate with the gender of CRC patients.
3.Operative management of type Ⅱ fracture of the distal clavicle
Chinese Journal of Orthopaedic Trauma 2002;0(04):-
Objective To introduce an operative method for the treatment of type Ⅱ fracture of distal clavicle. Methods The clavicle and coracoid proc ess were compressively fixed with screw in, and the coracoclavicular ligament wa s repaired in 24 cases of type Ⅱ fracture of the distal clavicle. Results The fractures healed in all the cases with good function of joint, and without screw loosening or traumatic arthritis. Conclusion The operative method is an ideal m anagement for the treatment of adult type Ⅱ fracture of distal clavicle, due t o its easy handling, reliable fixation, exact curative effects and less complica tions.

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