Effect of thyrotropin-releasing hormone on cerebral free radical reactions following acute brain injury in rabbits

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Effect of Radix Paeoniae Rubra on the expression of HO-1 and iNOS in rats with endotoxin-induced acute lung injury

Objective: To investigate the effect of Radix Paeoniae Rubra (RPR) on the expression of heme oxygenase (HO-1) and induced nitric oxide synthase (iNOS) in endotoxin-induced acute lung injury in rats and its protective mechanism. Methods: Forty Wistar rats were divided randomly into 5 groups with 8 rats in each group: saline control group (NS group), lipopolysaccharide group ( LPS group), RPR-treatment group, RPR-prevention group and Hemin group. The effect of RPR on protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid, malondialdehyde ( MDA ) content in the lung and the activity of serum NO were observed. Arterial blood was drawn for blood-gas analysis. The expression of HO-1 and iNOS in lung tissues was detected by immunohistochemitry and morphometry computer image analysis. The histological changes of the lung were observed under light microscope. Results: Compared with that in NS group, the expression of HO-1 and iNOS was markedly increased in LPS group (P<0.01). In RPR-treatment, RPR-prevention , and Hemin groups, the expression of iNOS was significantly lower, while the expression of HO-1 was higher than that in LPS group (P<0.05). The protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid, the content of MDA and the activity of serum NO in LPS group were significantly higher than those in NS group (P<0.01). There was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in the LPS group (P<0.01); these parameters of lung injury however, were significantly lower in RPR-treatment. RPR-prevention, and Hemin groups than LPS group (P<0. 05 or P< 0.01). The pathologic changes of lung tissues were substantially attenuated in RPR-treatment, RPR-prevention, and Hemin groups than LPS group. Conclusions: The high expression of HO-1 reflects an important protective function of the body during lipopolysaccharide-induced acute lung injury. The protective effect of RPR on lipopolysaccharide-induced acute lung injury is related to the inhibition of iNOS expression and the induction of HO-1 expression.     

Effect of Radix Paeoniae Rubra on the expression of HO-1 and iHOS in rats with endotoxin-induced acute lung injury

Objective ： To investigate the effect of Radix Paeoniae Rubra （RPR） on the expression of heme oxygenase （ HO- 1 ） and induced nitric oxide synthase （ iNOS ） in endotoxin- induced acute lung injury in rats and its protective mechanism. Methods： Forty Wistar rats were divided randomly into 5 groups with 8 rats in each group： saline control group （NS group ）, lipopolysaccharide group （LPS group）, RPR-treatment group, RPR-prevention group and Hemin group. The effect of RPR on protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid, malondialdehyde （MDA） content in the lung and the activity of serum NO were observed. Arterial blood was drawn for blood-gas analysis. The expression of HO-1 and iNOS in lung tissues was detected by immunohistochemitry and morphometry computer image analysis. The histological changes of the lung were observed under fight microscope. Results： Compared with that in NS group, the expression of HO-1 and iNOS was markedly increased in LPS group （P 〈0.01）. In RPR-treatment, RPR-prevention, and Hemin groups, the expression of iNOS was significantly lower, while the expression of HO-1 was higher than that in LPS group （P〈0.05）. The protein content, the ratio of neutrophiles in bronchouiveolar lavage fluid, the content of MDA and the activity of serum NO in LPS group were significantly higher than those in NS group （ P〈0.01 ）. There was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in the LPS group （P 〈0.01）; these parameters of lung injury however, were significantly lower in RPR-treatment, RPR- prevention, and Heroin groups than LPS group （P〈0.05 or P〈0.01 ）. The pathologic changes of lung tissues were substantially attenuated in RPR-treatment, RPR- prevention, and Hemin groups than LPS group. Conclusions ： The high expression of HO-1 reflects an important protective function of the body during lipopolysaccharide-induced acute lung injury. The acute lung injury is related to the inhibition of iNOS expression and the induction of HO-1 expression.     

Effects of low-level laser therapy on expression of TNF-α and TGF-β in skeletal muscle during the repair process

The aim of the present study was to determine the effect of low-level laser therapy (LLLT) on the expression of TNF-α and TGF-β in the tibialis anterior muscle of rats following cryoinjury. Muscle regeneration involves cell proliferation, migration and differentiation and is regulated by growth factors and cytokines. A growing body of evidence suggests that LLLT promotes skeletal muscle regeneration by reducing the duration of acute inflammation and accelerating tissue repair. Adult male Wistar rats (n = 35) were randomly divided into three groups: control group (no lesion, untreated, n = 5), cryoinjury without LLLT group (n = 15), and cryoinjury with LLLT group (n = 15). The injured region was irradiated three times a week using an AlGaInP laser (660 nm; beam spot 0.04 cm², output power 20 mW, power density 500 mW/cm², energy density 5 J/cm², exposure time 10 s). Muscle remodeling was evaluated at 1, 7 and 14 days (long-term) following injury. The muscles were removed and total RNA was isolated using TRIzol reagent and cDNA synthesis. Real-time polymerase chain reactions were performed using TNF-α and TGF-β primers; GAPDH was used to normalize the data. LLLT caused a decrease in TNF-α mRNA expression at 1 and 7 days following injury and in TGF-β mRNA expression at 7 days following cryoinjury in comparison to the control group. LLLT modulated cytokine expression during short-term muscle remodeling, inducing a decrease in TNF-α and TGF-β.     

Effects of photobiomodulation therapy and topical non-steroidal anti-inflammatory drug on skeletal muscle injury induced by contusion in rats—part 1: morphological and functional aspects

Musculoskeletal injuries are very frequent and are responsible for causing pain and impairment of muscle function, as well as significant functional limitations. In the acute phase, the most prescribed treatment is with non-steroidal anti-inflammatory drugs (NSAIDs), despite their questionable effectiveness. However, the use of photobiomodulation therapy (PBMT) in musculoskeletal disorders has been increasing in the last few years, and this therapy appears to be an interesting alternative to the traditional drugs. The objective of the present study was to evaluate and compare the effects of PBMT, with different application doses, and topical NSAIDs, under morphological and functional parameters, during an acute inflammatory process triggered by a controlled model of musculoskeletal injury induced via contusion in rats. Muscle injury was induced by means of a single trauma to the animals’ anterior tibialis muscle. After 1 h, the rats were treated with PBMT (830 nm; continuous mode, with a power output of 100 mW; 3.57 W/cm²; 1 J–35.7 J/cm², 3 J–107.1 J/cm², and 9 J–321.4 J/cm²; 10, 30, and 90 s) or diclofenac sodium for topical use (1 g). Morphological analysis (histology) and functional analysis (muscle work) were performed, 6, 12, and 24 h after induction of the injury. PBMT, with all doses tested, improved morphological changes caused by trauma; however, the 9 J (321.4 J/cm²) dose was the most effective in organizing muscle fibers and cell nuclei. On the other hand, the use of diclofenac sodium produced only a slight improvement in morphological changes. Moreover, we observed a statistically significant increase of muscle work in the PBMT 3 J (107.1 J/cm²) group in relation to the injury group and the diclofenac group (p < 0.05). The results of the present study indicate that PBMT, with a dose of 3 J (107.1 J/cm²), is more effective than the other doses of PBMT tested and NSAIDs for topical use as a means to improve morphological and functional alterations due to muscle injury from contusion.     

Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.     

Effects of photobiomodulation therapy and topical non-steroidal anti-inflammatory drug on skeletal muscle injury induced by contusion in rats—part 2: biochemical aspects

Muscle injuries trigger an inflammatory process, releasing important biochemical markers for tissue regeneration. The use of non-steroidal anti-inflammatory drugs (NSAIDs) is the treatment of choice to promote pain relief due to muscle injury. NSAIDs exhibit several adverse effects and their efficacy is questionable. Photobiomodulation therapy (PBMT) has been demonstrated to effectively modulate inflammation induced from musculoskeletal disorders and may be used as an alternative to NSAIDs. Here, we assessed and compared the effects of different doses of PBMT and topical NSAIDs on biochemical parameters during an acute inflammatory process triggered by a controlled model of contusion-induced musculoskeletal injury in rats. Muscle injury was induced by trauma to the anterior tibial muscle of rats. After 1 h, rats were treated with PBMT (830 nm, continuous mode, 100 mW of power, 35.71 W/cm²; 1, 3, and 9 J; 10, 30, and 90 s) or diclofenac sodium (1 g). Our results demonstrated that PBMT, 1 J (35.7 J/cm²), 3 J (107.1 J/cm²), and 9 J (321.4 J/cm²) reduced the expression of tumor necrosis factor alpha (TNF-α) and cyclooxygenase-2 (COX-2) genes at all assessed times as compared to the injury and diclofenac groups (p < 0.05). The diclofenac group showed reduced levels of COX-2 only in relation to the injury group (p < 0.05). COX-2 protein expression remained unchanged with all therapies except with PBMT at a 3-J dose at 12 h (p < 0.05 compared to the injury group). In addition, PBMT (1, 3, and 9 J) effectively reduced levels of cytokines TNF-α, interleukin (IL)-1β, and IL-6 at all assessed times as compared to the injury and diclofenac groups (p < 0.05). Thus, PBMT at a 3-J dose was more effective than other doses of PBMT and topical NSAIDs in the modulation of the inflammatory process caused by muscle contusion injuries.     

Effect of NF-κB modulated PTH expression on hypocalcemia in acute pancreatitis

低钙血症是重症急性胰腺炎(SAP)的重要并发症之一,与疾病的严重程度和预后密切相关,其产生和发展的确切机制未明.     

Histological, enzymohistochemical and biomechanical observation of skeletal muscle injury in rabbits

OBJECTIVE: To explore the pathophysiological and biomechanical features of skeletal muscular injury for providing a rational basis for its treatment, prevention and rehabilitation. METHODS: In 70 adult rabbits, the left tibialis anterior (TA) muscle was stretched to injury, while the right TA muscle served as control. Histological, enzymohistochemical and biomechanical changes were observed on days 0, 1, 2, 3, and 7 after injury. Cytochrome oxidase (CCO), acid phosphatase (ACP), ATPase, succinate dehydrogenase (SDH), malate dehydrogenase (MDH), NADH-diaphorase (NADHD), glutamatedehydrogenase (GDH), alpha-glycerophosphate dehydrogenase (alpha-GPD) and lactate dehydrogenase (LDH) were measured. The examined biomechanical parameters included maximal contractile force, ultimate load, length, energy absorption, tangent stiffness, and rupture site. RESULTS: Partial or complete rupture of TA muscle occurred near the muscle-tendon junction. There was an intense inflammatory reaction on day 1 and 2 after injury. Endomysium fibrosis and myotube formation were observed on day 3, and developed further on day 7. The activity of cell oxidases (CCO, ATPase, MDH, alpha-GPD, SDH, NADHD and GDH) showed a significant drop from day 0 to 2, and resumed with different levels on day 3. The increment of enzymatic activities continued on day 7 and the levels of NADHD and alpha-GPD reached to the levels of control muscle. Maximal contractile force was 70.17%+/-3.82% of controls immediately after injury, 54.82%+/-3.09% at 1 day, 66.41%+/-4.36% at 2 days, 78.39%+/-4.90% at 3 days and 93.64%+/-5.02% at 7 days. Ultimate load was 85.78%+/-7.54% of controls at the moment of injury, 61.44%+/-5.91% at 1 day, 49.17%+/-4.26% at 2 days, 64.43%+/-5.02% at 3 days, and 76.71%+/-6.46% at 7 days. CONCLUSIONS: Endomysium fibrosis and scar formation at the injured site are responsible for frequent recurrence of skeletal muscle injury. Recovery of tensile load slower than that of maximal contractile force may be another cause. Whether the injured muscle returns to normal exercise is mainly determined by the tensility on which the muscle-tendon can bear rather than the maximal contractile force.     

Effect of NF-κB modulated PTH expression on hypocalcemia in acute pancreatitis

低钙血症是重症急性胰腺炎(SAP)的重要并发症之一,与疾病的严重程度和预后密切相关,其产生和发展的确切机制未明.     

Effect of isoflurane on expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA In the hippocamapus of immature rats

Obiective To investigate the effect ofisoflurane on expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA in the hippocampus of immature rats.Methods sixty-four 7-clay-old SD rats were randomly assigned into 2 groups(n=32 each):control group(group C)and isoflurane group(group S).group S was exposed to 1.5% isoflurane for 6 h while group C to air.Fore animals were killed before anesthesia(T0,baseline),at 2,4,6 h(T1-3)of isoflurane anesthesia and 4,6,12 and 24 h after anesthesia(T4-7).The hippocampi were immediately removed for determimation of the expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA by RT-PCR.Results Compared with group C,the expression of IL-1β mRNA at T1-5,IL-6 mRNA at T2.3 and TNF-α mRNA at T1-6 in the hippocampus was upregulated in group S.Conclusion The expression of IL-1β mRNA,IL-6 mRNA and TNF-β mRNA was elevated in the hippocampus of immature rats after being exposed to isoflurane.     

Effect of isoflurane on expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA In the hippocamapus of immature rats

Obiective To investigate the effect ofisoflurane on expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA in the hippocampus of immature rats.Methods sixty-four 7-clay-old SD rats were randomly assigned into 2 groups(n=32 each):control group(group C)and isoflurane group(group S).group S was exposed to 1.5% isoflurane for 6 h while group C to air.Fore animals were killed before anesthesia(T0,baseline),at 2,4,6 h(T1-3)of isoflurane anesthesia and 4,6,12 and 24 h after anesthesia(T4-7).The hippocampi were immediately removed for determimation of the expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA by RT-PCR.Results Compared with group C,the expression of IL-1β mRNA at T1-5,IL-6 mRNA at T2.3 and TNF-α mRNA at T1-6 in the hippocampus was upregulated in group S.Conclusion The expression of IL-1β mRNA,IL-6 mRNA and TNF-β mRNA was elevated in the hippocampus of immature rats after being exposed to isoflurane.     

Dexmedetomidine protects against ischemia–reperfusion injury in rat skeletal muscle

Background

Dexmedetomidine (DEX) has been shown to decrease ischemia–reperfusion (I/R) injury in kidney and brain tissues. In this study, the effects of DEX were evaluated in skeletal muscle during I/R injury.

Materials and methods

Animals were divided into four groups: sham-operated (sham group), saline + I/R, DEX + I/R, and α-tocopherol + I/R groups. Hind limb ischemia was induced by clamping the common femoral artery and vein. After 4 h of ischemia, the clamp was removed and the animals underwent 2 h of reperfusion. Animals in the drug treatment group received DEX or α-tocopherol by intraperitoneal injection 1 h before reperfusion. We measured plasma concentrations of interleukin 1β and tumor necrosis factor α levels using an enzyme-linked immunosorbent assay. The right gastrocnemius muscle was harvested and immediately stored at −80°C for the assessment of superoxide dismutase (SOD) and catalase (CAT) activities as well as glutathione (GSH), malondialdehyde (MDA), and protein oxidation (PO) levels. DEX (25 μg/kg) and normal saline (10 mL/kg) were administered by intraperitoneal injection 1 h before reperfusion.

Results

Plasma tumor necrosis factor α or interleukin 1β levels increased significantly in the I/R group (P < 0.01 compared with sham group) and decreased significantly in the DEX group (P < 0.01 compared with I/R group). Muscle tissues of the I/R group had significantly decreased SOD, GSH, and CAT activities and increased levels of MDA and PO content compared with the sham group. The activity of antioxidant enzymes in the DEX + I/R group was greatly elevated compared with that in the I/R group (SOD, 1.068 ± 0.120 versus 0.576 ± 0.072 U/mg protein; GSH, 2.436 ± 0.144 versus 1.128 ± 0.132 μmol/g; and CAT, 69.240 ± 6.456 versus 31.884 ± 6.312 U/mg protein; P < 0.01), whereas the levels of MDA and PO content were clearly reduced (23.268 ± 3.708 versus 53.604 ± 5.972 nmol/g protein and 1.908 ± 0.192 versus 5.208 ± 0.612 nmol/mg protein, respectively; P < 0.01). Moreover, DEX exhibited more potent antioxidant activity than vitamin E in the skeletal muscle I/R.

Conclusions

We found that DEX exhibits protective effects against skeletal muscle I/R injury. These results underscore the necessity of human studies with DEX to determine if it is beneficial for preventing skeletal muscle I/R injury.     

The impact of catecholamines on skeletal muscle following massive burns: Friend or foe?

Profound skeletal muscle wasting in the setting of total body hypermetabolism is a defining characteristic of massive burns, compromising the patient’s recovery and necessitating a protracted period of rehabilitation. In recent years, the prolonged use of the non-selective beta-blocker, propranolol, has gained prominence as an effective tool to assist with suppressing epinephrine-dependent burn-induced hypermetabolism and by extension, blunting muscle catabolism. However, synthetic β-adrenergic agonists, such as clenbuterol, are widely associated with the promotion of muscle growth in both animals and humans. Moreover, experimental adrenodemedullation is known to result in muscle catabolism. Therefore, the blunting of muscle β-adrenergic signaling via the use of propranolol would be expected to negatively impair muscle protein homeostasis. This review explores these paradoxical observations and identifies the manner by which propranolol is thought to exert its anti-catabolic effects in burn patients. Moreover, we identify potential avenues by which the use of beta-blocker therapy in the treatment of massive burns could potentially be further refined to promote the recovery of muscle mass in these critically ill patients while continuing to ameliorate total body hypermetabolism.     

Effects of low-level laser therapy on ROS homeostasis and expression of IGF-1 and TGF-β1 in skeletal muscle during the repair process

The aim of the present study was to determine the effects of low-level laser therapy (LLLT) on the homeostasis of reactive oxygen species (ROS) and expression of IGF-1 and TGF-β1 in the gastrocnemius muscles of rats following contusion. Muscle regeneration involves cell proliferation, migration, and differentiation and is regulated by growth factors. A growing body of evidence suggests that LLLT promotes skeletal muscle regeneration and accelerates tissue repair. Adult male Sprague-Dawley rats (n?=?96) were randomly divided into three groups: control group (no lesion, untreated, n?=?6), contusion group (n?=?48), and contusion-plus-LLLT group (n?=?42). Gallium aluminum arsenide (GaAlAs) laser irradiation (635 nm; beam spot, 0.4 cm²; output power, 7 mW; power density, 17.5 mW/cm²; 20 min) was administered to the gastrocnemius contusion for 20 min daily for 10 days. Muscle remodeling was evaluated at 0 h and 1, 2, 3, 7, 14, 21, and 28 days after injury. Hematoxylin and eosin and Van Gieson staining were used to evaluate regeneration and fibrosis; muscle superoxide dismutase (SOD) and malondialdehyde (MDA) were detected via biochemical methods; expression of transforming growth factor beta-1 (TGF-β1) and insulin-like growth factor-1 (IGF-1) were investigated via immunohistochemistry. The results showed that LLLT markedly promoted the regeneration of muscle and reduced scar formation. LLLT also significantly enhanced muscle SOD activity and significantly decreased muscle MDA levels 1, 2, and 3 days after injury. LLLT increased the expression of IGF-1 2, 3, and 7 days after injury and decreased the expression of IGF-1 21 and 28 days after injury. LLLT decreased the expression of TGF-β1 3 and 28 days after injury but increased expression at 7 and 14 days after injury. Our study showed that LLLT could modulate the homeostasis of ROS and of the growth factors IGF-1 and TGF-β1, which are known to play important roles in the repair process. This may constitute a new preventive approach to muscular fibrosis.     

Effect of 830 nm low-level laser therapy in exercise-induced skeletal muscle fatigue in humans

This study aimed to investigate the effect of 830 nm low-level laser therapy (LLLT) on skeletal muscle fatigue. Ten healthy male professional volleyball players entered a crossover randomized double-blinded placebo-controlled trial. Active LLLT (830 nm wavelength, 100 mW output, spot size 0.0028 cm², 200 s total irradiation time) or an identical placebo LLLT was delivered to four points on the biceps humeri muscle immediately before exercises. All subjects performed voluntary biceps humeri contractions with a load of 75% of the maximum voluntary contraction (MVC) force until exhaustion. After active LLLT the mean number of repetitions was significantly higher than after placebo irradiation [mean difference 4.5, standard deviation (SD) ± 6.0, P = 0.042], the blood lactate levels increased after exercises, but there was no significant difference between the treatments. We concluded that 830 nm LLLT can delay the onset of skeletal muscle fatigue in high-intensity exercises, in spite of increased blood lactate levels.     

Effect of 830 nm low-level laser therapy applied before high-intensity exercises on skeletal muscle recovery in athletes

Our aim was to investigate the immediate effects of bilateral, 830 nm, low-level laser therapy (LLLT) on high-intensity exercise and biochemical markers of skeletal muscle recovery, in a randomised, double-blind, placebo-controlled, crossover trial set in a sports physiotherapy clinic. Twenty male athletes (nine professional volleyball players and eleven adolescent soccer players) participated. Active LLLT (830 nm wavelength, 100 mW, spot size 0.0028 cm², 3–4 J per point) or an identical placebo LLLT was delivered to five points in the rectus femoris muscle (bilaterally). The main outcome measures were the work performed in the Wingate test: 30 s of maximum cycling with a load of 7.5% of body weight, and the measurement of blood lactate (BL) and creatine kinase (CK) levels before and after exercise. There was no significant difference in the work performed during the Wingate test (P?>?0.05) between subjects given active LLLT and those given placebo LLLT. For volleyball athletes, the change in CK levels from before to after the exercise test was significantly lower (P?=?0.0133) for those given active LLLT (2.52 U l^?1 ± 7.04 U l^?1) than for those given placebo LLLT (28.49 U l^?1 ± 22.62 U l^?1). For the soccer athletes, the change in blood lactate levels from before exercise to 15 min after exercise was significantly lower (P?<?0.01) in the group subjected to active LLLT (8.55 mmol l^?1 ± 2.14 mmol l^?1) than in the group subjected to placebo LLLT (10.52 mmol l^?1 ± 1.82 mmol l^?1). LLLT irradiation before the Wingate test seemed to inhibit an expected post-exercise increase in CK level and to accelerate post-exercise lactate removal without affecting test performance. These findings suggest that LLLT may be of benefit in accelerating post-exercise recovery.     

Effect of spinal cord injury on iNOS and Bcl-2 gene expression in spermatogenic cell of male rats

Effect of spinal cord injury on iNOS and Bcl-2 gene expression in spermatogenic cell of male rats