Zhi-hua Li

Publications (2)0.86 Total impact

• Article: [Effects of depressive disorder on monocytic expression of CD(40) and plasma IL-8 concentration in senile coronary heart disease patients].

  Chun-Fu Wan, Zhi-Hua Li, Guan-Jie Xu, Shun-Suo Liu, Xiao-Yong Qi
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  ABSTRACT: To observe the monocytic expression of CD(40) and plasma IL-8 concentration in senile CHD (coronary heart disease) patients with depressive disorder and examine the effects of immunological factors in depressive disorder and CHD. A total of 100 senile CHD patients (> 60 yr old) were divided into 3 group: control group (A, n = 30), depression score ≤ 20 & anxiety score ≤ 6; therapy group (B, n = 35), depression score ≥ 30 & anxiety score ≤ 6, psychological evaluations with HAMD (Hamilton depression rating scale) from Day 1 pre-operation to Day 7 post-operation; non-therapy group (C, n = 35), depression score ≥ 30 & anxiety score ≤ 6. They underwent the same operation: lumbar decompression & fusion, stripping of great saphenous vein and repair of indirect hernia. At Day 1 pre-operation and Day 7 post-operation, 2 ml venous blood was drawn for the detection of monocytic expression of CD(40) and plasma concentration of IL-8 (interleukin-8). Depressive value of Group B at post-operation was lower than that at pre-operation and Group C ((25.1 ± 2.9) vs (33.2 ± 1.4) & (34.2 ± 0.8), P < 0.05); the pre-operative expression of CD(40) of Group A was lower than the other groups ((123 ± 18) vs (197 ± 23) & (204 ± 26), P < 0.05). And Group B at post-operation was lower than Group C ((147 ± 19) vs (212 ± 18), P < 0.05); the pre-operative concentration of IL-8 was lowest in Group A ((85 ± 16) ng/L vs (151 ± 18) ng/L & (164 ± 22) ng/L, P < 0.05). And Group B at post-operation was lower than Group C ((158 ± 19) ng/L vs (197 ± 24) ng/L, P < 0.05). There were significantly positive correlations between depression scores, the expression of CD(40) and the plasma concentration of IL-8. Depressive disorders elevate the monocytic expression of CD(40) and raise the plasma concentration of IL-8 in senile CHD patients. Some immunological factors may play a important role in depressive disorder and CHD.
  Zhonghua yi xue za zhi 09/2011; 91(35):2459-63.
• Article: Different effects of isoflurane and sevoflurane on cytotoxicity.

  Qiu-jun Wang, Ke-zhong Li, Shang-long Yao, Zhi-hua Li, Shun-suo Liu
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  ABSTRACT: Isoflurane, a commonly used inhaled anesthetic, induces apoptosis in primary rat cortical neurons of rat in a concentration- and time-dependent manner by an unknown mechanism. We hypothesized that isoflurane induced apoptosis by causing abnormal calcium release from the endoplasmic reticulum (ER) via activation of inositol 1, 4, 5-trisphosphate (IP(3)) receptors. Sevoflurane has a reduced ability to disrupt intracellular calcium homeostasis and is a less potent cytotoxic agent. This study examined and compared the cytotoxic effects of isoflurane and sevoflurane on rat primary cortical neurons and their relationship with disruption of intracellular calcium homeostasis and production of reactive oxygen species (ROS). Primary rat cortical neurons were treated with the equivalent of 1 minimal alveolar concentration (MAC) of isoflurane and sevoflurane for 12 hours. MTT reduction and LDH release assays were performed to evaluate cell viability. Changes of calcium concentration in the cytosolic space, [Ca(2+)](c), and production of ROS were determined after exposing primary rat cortical neurons to isoflurane and sevoflurane. We also determined the effects of IP(3) receptor antagonist xestospongin C on isoflurane-induced cytotoxicity and calcium release from the ER in primary rat cortical neurons. Isoflurane at 1 MAC for 12 hours induced cytotoxicity in primary rat cortical neurons, which was also associated with a high and fast elevation of peak [Ca(2+)](c). Xestospongin C significantly ameliorated isoflurane cytotoxicity in primary cortical neurons, as well as inhibited the calcium release from the ER in primary cortical neurons. Isoflurane did not induce significant changes of ROS production in primary rat cortical neurons. Sevoflurane, at equivalent exposure to isoflurane, did not induce similar cytotoxicity or elevation of peak [Ca(2+)](c) in primary rat cortical neurons. These results suggested that isoflurane induced elevation in [Ca(2+)](c), partially via elevated activity of IP(3) receptors, which rendered cells vulnerable to isoflurane neurotoxicity. ROS production was not involved in isoflurane-induced neurotoxicity. Sevoflurane, at an equivalent exposure to isoflurane, did not induce similar elevations of [Ca(2+)](c) or neurotoxicity in primary cortical neurons of rat.
  Chinese medical journal 03/2008; 121(4):341-6. · 0.86 Impact Factor