scispace - formally typeset
Search or ask a question
JournalISSN: 1000-6834

Chinese journal of applied physiology 

Chinese Medical Association
About: Chinese journal of applied physiology is an academic journal published by Chinese Medical Association. The journal publishes majorly in the area(s): Medicine & Internal medicine. It has an ISSN identifier of 1000-6834. Over the lifetime, 1214 publications have been published receiving 2674 citations. The journal is also known as: Chinese Journal of Applied Physiology.


Papers
More filters
Journal Article
X H Deng1, J Shi, S Q Luo, C He, C H Wang, C L Lu 
TL;DR: CNTF significantly attenuates denervation-reduced skeletal muscle atrophy and dysfunction in SD rats, act an evident myotrophic effect on denervated skeletal muscle and may be exerted in a dosage dependent manner and varies with muscle type.
Abstract: Aim The trophic effect of CNTF on skeletal muscle atrophy and dysfunction reduced by denervation was investigated in SD rats Methods SD rats transected sciatic nerve in right side hind limbs were injected CNTF subcutaneously for 20 days Skeletal muscle wet weights, protein contents, muscle fiber cross-sectional areas, contract properties and degree of hind limb abnormalities were observed in the rats Results (1) Administrating of CNTF (02 mg/kg) in sciatic nerve transected SD rats attenuated denervation-induced skeletal muscle fiber atrophy evidently, resulted in gastrocnemius in injury side an obvious increase in contract function, prevented the loss of weights and protein in denervated skeletal muscle, and ameliorated abnormalities in sciatic nerve cut limbs remarkably (2) The myotrophic effect of 02 mg/kg CNTF is more effective than 005 mg/kg (3) The sensitivity to CNTF varied in muscles of different type; slow twitch muscle (soleus muscle) reacted to CNTF stronger and quicker than twitch muscle (extensor digitorum longus) Conclusion CNTF significantly attenuates denervation-reduced skeletal muscle atrophy and dysfunction in SD rats, act an evident myotrophic effect on denervated skeletal muscle And this effect may be exerted in a dosage dependent manner and varies with muscle type

36 citations

Journal Article
TL;DR: Destruction of mitochondrial structure and function may be of great significance in the development of impaired cardiac function in the heat stress.
Abstract: Aim: In order to elucidate the mechanism of cardiomyocyte injury in heat stress, the changes of oxidative phosphorylation and calcium metalolism in cardiac mitochondria of heatexposed Wistar rats were observed. The changes of mitochondrial permeability transition and its pathological significance were studied as well. Methods: The respiratory function of mitochondria was measured by Klark oxgenelectrode polarography; Myocardial ATP content and activity of Ca 2+ ATPase in mitochondria were analyzed with bioluminescent method; Mitochondrial Ca 2+ content was assayed by ICP; PT was measured using spectrophotometer. Results: The respiratory control rate (RCR) and oxidative phosphorylation efficiency (P/O) were decreased gradually as rectal temperature (Tr) increased. The activity of Ca 2+ ATPase and Ca 2+ content were also reduced. Exposing to the Ca 2+ overload and oxidative stress, mitochondrial PT altered markedly. Ruthenium red and SOD could prevent the changes of mitochondrial PT. Conclusion: Destruction of mitochondrial structure and function may be of great significance in the development of impaired cardiac function in the heat stress.

27 citations

Journal Article
TL;DR: It is demonstrated that safflower injection could activate endoplasmic reticulum stress-induced apoptosis and especially promote apoptosis in pulmonary vascular smooth muscle cells.
Abstract: Objective To explore the effects of safflower injection on prevention and treatment of hypoxic pulmonary hypertension and clarify the function of the endoplasmic reticulum stress apoptosis pathway during the process. Methods Thirty male SD rats were randomly grouped as normal control group, hypoxia-hypercapnia group and hypoxia+safflower group. The latter two groups were put in the cabin with oxygen concentration ranged from 9% to 11% and carbon dioxide concentration from 5% to 6%. The pulmonary artery pressure and the index of right ventricular hypertrophy were determined after hypoxia exposure (8 h/dx28 d). Changes in morphology of lung tissue were observed by electron microscopy. To explore the possible mechanisms, we also detected apoptosis and apoptosis-related genes/proteins in lung tissue by TUNEL reactivity and PCR and Western blot. Results Compared with the normal control group, pulmonary artery pressure and the index of right ventricular hypertrophy in hypoxia group were 45% and 33.4% higher, respectively. Tiny blood vessel wall of lungs was thickened and edema, and proliferation of collagen fibers was obvious under the electron microscope. TUNEL staining of apoptotic cells in lung tissues showed more high brightness green fluorescence (+-++), but less green fluorescence showed in the pulmonary vascular smooth muscle cell layer, and apoptosis index (AI) value was 150% higher; gene and protein expression levels of endoplasmic reticulum stress pathway were increased. Compared with hypoxia-hypercapnia group, pulmonary artery pressure and the index of right ventricular hypertrophy in the hypoxia+safflower group were 18% and 15.6% lower, respectively; collagen fibers were decreased, and smooth muscle cells and epithelial cells were got apoptotic-like changes under the electron microscope. TUNEL staining of apoptotic cells in lung tissues showed brighter green fluorescence (++-+++); the high brightness green fluorescence showed in pulmonary vascular smooth muscle cell layer, and apoptotic index (Al) value was 40% higher; gene and protein expressions of endoplasmic reticulum stress pathway were significantly upregulated. Conclusion Our findings demonstrate that safflower injection could activate endoplasmic reticulum stress-induced apoptosis and especially promote apoptosis in pulmonary vascular smooth muscle cells.

19 citations

Journal Article
TL;DR: Observations provide evidence for beneficial effect of lycopene supplementation in rotenone-induced PD and suggest therapeutic potential in neurodegenerative diseases involving accentuated oxidative stress.
Abstract: Objective To investigate the neuroprotective potential of lycopene on oxidative stress and neurobehavioral abnormalities in rotenone induced Parkinson' disease (PD). Methods Forty adult C57BL/6 mice were randomly divided into four groups (n = 10): control, lycopene (10 mg/kg body weight, orally), rotenone (3 mg/kg bw, intraperitoneally) and rotenone plus lycopene, which were sacrificed for 5 weeks. The spectrophotometry was used to determine the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the content of malondialdehyde (MDA) in substantia nigra and right striatum. At the same time, the number of tyrosine hydroxylase (TH), alpha-synuclein (alpha-SYN) and microtubule-associated protein 3 light chain (LC3-B) positive neurons were estimated by immunohistochemistry. We also examined neurobehavioral abnormalities by WT-200 water maze. Results Rotenone administration increased the MDA levels and significantly decreased the activities of SOD, GSH-Px and CAT. However, lycopene administration to the rotenone treated animals increased the activities of SOD, GSH-Px and CAT when compared to rotenone treated animals in substantia nigra and right striatum. The cognitive and motor deficits in rotenone administered animals, which were reversed on lycopene treatment. Along with this, the number of TH decreased, alpha-SYN increased and LC3-B positive neurons increased in rotenone administered animals, which were reversed on lycopene treatment. Conclusion Collectively, these observations provide an evidence for beneficial effect of lycopene supplementation in rotenone-induced PD and suggest therapeutic potential in neurodegenerative diseases involving accentuated oxidative stress.

17 citations

Journal Article
Hua Zhou1, De-Hu Kong, Rong Ma, Dao-Ping Ke, Jin-Lan Hu, Jie Song 
TL;DR: SOC activated by store depletion are present in rat colonic smooth muscle cells and it is proved the existence of such Ca2+ channels in excitable cells.
Abstract: AIM To study whether store-operated Ca2+ channel (SOC) is present in rat colonic smooth muscle cells. METHODS Intracellular Ca2+ ([Ca2+]i) changes induced by thapsigargin- or caffeine-activated SOC channel were measured in enzymatically dissociated rat colonic smooth muscle cells with the fluorescent indicator Fura-2/AM. RESULTS In the absence of external Ca2+ , the sarco-endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (1 micromol/L) and ryanodine receptor (RyR) activator caffeine both transiently elevated [Ca2+]i from (68.32 +/- 3.43) nmol/L to (240.85 +/- 12.65 ) nmol/L, (481.25 +/- 34.77) nmol/L. A subsequent reintroduction of Ca2+ into the extracellular solution resulted in [Ca2+]i further elevated to (457.55 +/- 19.80) nmol/L, (1005.93 +/- 54.62) nmol/L; (643.88 +/- 34.65) nmol/L, (920.16 +/- 43.25) nmol/L, respectively. And the elevated response was blocked by lanthanum (1 mmol/L), but was insensitive to L-type voltage calcium channels blocker verapamil and membrane depolarization. CONCLUSION SOC activated by store depletion are present in rat colonic smooth muscle cells. And we further prove the existence of such Ca2+ channels in excitable cells.

15 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
2022143
202012
201936
201864
201743
201630