Browsing by Author "Chen, Ing-Ho"

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Effects of freshwater clam extract on fracture induced inflammation at early stage
(2017-11-01)
Yeh, Kuang-Ting
;
Wu, Wen-Tien
;
Subeq, Yi-Maun
;
Niu, Chi-Chien
;
Liao, Kuang-Wen
The inflammatory process after traumatic fracture and soft tissue injury includes release of inflammatory cytokines and activated polymorph nuclear cells (PMN) that can cause subsequent affected limbs delayed healing and vital organ complications. Analgesics have good effect on relief of the symptom but may cause further burden for hepatic and renal metabolism. Freshwater clam extract (FCE) has been demonstrated to suppress the release of the pro-inflammatory cytokine tumor necrosis factor-alpha production after hemorrhagic shock, and decrease the level of liver injury marker in rats. The aim of the present study was to determine whether FCE is able to affect the inflammation induced by unilateral tibial fracture in a rat model. The rats were randomly divided into control, fracture, FCE and fracture with FCE groups. The fracture group received left tibia and fibula shaft fractures using a consistent three point bending method. For the fracture with FCE group, FCE (40 mg/kg) was administered orally after fracture. Their physiological changes were continuously monitored for 48 h. Blood samples were extracted from the femoral arterial catheter at 1, 3, 6, 9, 12, 18, 24 and 48 h after fracture. In comparison with fracture group, those whom were fed with FCE had more stable heart rate frequency, lower central temperature at the initial h, and lower serum level of the proinflammatory cytokines and muscle damage markers induced by fracture. FCE was also associated with decreased recruitment of inflammatory cells in the adjacent soft tissue. Thus, the present results suggest that FCE could decrease fracture induced inflammation reaction and have beneficial regulatory effect on post inflammatory response.
Non-Steroid Anti-Inflammatory Drugs Are Better than Acetaminophen on Fever Control at Acute Stage of Fracture
(2015-10-02)
Yeh, Kuang-Ting
;
Wu, Wen-Tien
;
Subeq, Yi-Maun
;
Niu, Chi-Chien
;
Liao, Kuang-Wen
In addition to adequate surgical fixation and an aggressive rehabilitation program, pain relief is one of the most critical factors in the acute stage of fracture treatment. The most common analgesics are nonsteroid anti-inflammatory drugs and Acetaminophen, both of which relieve pain and reduce body temperature. In clinical experiences, they exhibit effective pain control; however, their influence on body temperature remains controversial. This study is aimed at determining the effects of analgesics at the acute stage of traumatic fracture by performing a clinical retrospective study of patients with fractures and a fracture animal model. The retrospective study revealed that, in the acetaminophen group, the mean value of postmedication body temperature (BT) was significantly higher than that of the premedication BT. The change in BT was highly related with the medication rather than other risk factors. Forty eight 12-week-old male Wistar rats were divided into 6 groups: a control group, fracture group, fracture-Acetaminophen group, Acetaminophen group, fracture-Arcoxia group, and Arcoxia group. Fracture rats were prepared by breaking their unilateral tibia and fibula. Their inflammation conditions were evaluated by measuring their serum cytokine level and their physiological status was evaluated by estimating their central temperature, heart rate, and mean blood pressure. The hepatic adverse effects were assessed by measuring the serum levels of aspartate aminotransferase (sGOT) and alanine aminotransferase (sGPT). The central temperature in the fracture-Acetaminophen group exceeded that in the groups fed normal saline water or Arcoxia. Accumulated hepatic injury was presented as steadily ascending curves of sGOT and sGPT. Inflammation-related cytokine levels were not higher in the Acetaminophen fracture group and were significantly lower in the fracture-Arcoxia group. Fever appeared to be aggravated by acetaminophen and more related to the elevation of hepatic enzymes than to the change in the inflammation-related cytokines. We suggest that acetaminophen may aggravate fever at the acute stage of fracture. This response is highly related to the accumulated and exacerbated side effects of hepatitis that are caused by the medication and trauma.