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Jiu-hua Cheng

Publications and source records attributed to Jiu-hua Cheng.

2 recordsLinked to original sources

[The inhibiting effect of niflumic acid on airway hyperresponsiveness in asthmatic mice].

OBJECTIVE: To evaluate the inhibiting effect of niflumic acid (NFA), an inhibitor of calcium-activated chloride channel (ClCa) on airway epithelium, on the airway hyperresponsiveness in asthmatic mice. METHODS: BALB/c mice were randomly divided into an asthma group (A group), a NFA prevention asthmatic group (B group) and a sham-challenged group (C group). The airway pressure time index (APTI) and the content of ET-1 and NO in bronchoalveolar lavage fluid (BALF) in all groups were measured. With the isolated tracheal rings with integral epithelium or epithelium removed from the asthma group (A(1) group and A(2) group) and the sham-challenged group (C(1) group and C(2) group), the contractile responsiveness of various rings to methacholine (mACh) was examined, and its change was observed when the rings were exposed to NFA beforehand. RESULTS: Compared with A group (1.62 +/- 0.14), the APTI in B group (1.21 +/- 0.07) was reduced remarkably (P < 0.01), and the contents of ET-1 [(103 +/- 9) ng/L] and NO [(48.5 +/- 3.2) micromol/L] in BALF of A group were significantly higher than those in B group, [(53 +/- 5) ng/L, (23.7 +/- 2.5) micromol/L (P < 0.01), respectively]. The ratios of maximum contractility in A(1), A(2), C(1) and C(2) groups were (3.79 +/- 0.44), (2.15 +/- 0.21), (1.26 +/- 0.14) and (2.06 +/- 0.18), respectively. The contractility of A(1) group was highest among all groups (all P < 0.01), but could be effectively decreased by NFA. CONCLUSIONS: By inhibiting the special ClCa on the airway epithelium, NFA can inhibit the production of ET-1 and NO by epithelium and thus exert preventive effect on airway hyperresponsiveness in asthma.

Animals↗

[Decrease in tetanic tension in 4-week tail-suspended rat soleus and analysis of its underlying mechanisms].

Objective. To observe the dynamic changes in tetanic tension in 4-week tail-suspended rat soleus (SOL) and extensor digitorum longus muscle (EDL) and to elucidate its underlying mechanisms. Method. After 4 weeks of tail suspension SOL and EDL of the rats were isolated and perfused. Their isometric twitch and tetanic tensions were recorded. Result. Atrophy occurred in the SOL, but not in the EDL. The maximum twitch tension (Pt) decreased significantly and was more dependent on stimulation voltage in SOL of tail-suspended rat. Time to maximum twitch tension (TPT) and time from maximum twitch tension to half relaxation (TR50) were reduced in the SOL. Pt also decreased in the EDL, but TPT and TR50 did not change in the EDL. The maximum tetanic tension reduced in SOL and EDL of tail-suspended rats. The decline rate of tetanic tension in SOL was faster than the control. The profile of tetanic contraction curve in atrophic SOL approached that in EDL. Conclusion. The above results suggested that the underlying mechanisms of reduced maximum twitch and tetanic tension in 4-week tail-suspended rat SOL may involve the reduction in number of cross-bridge per cross-section area or force produced per cross-bridge. The rapid decline rate in atrophic SOL may be related to the shift in myosin heavy chain and troponin I isoforms or to decrease in excitability.

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