The in vitro antiapoptotic effect of lithium chloride in mouse thymocytes

The effects of lithium chloride (LiC1) on thymocyte apoptosis induced by dexamethasone (DEX) were investigated. When primary culture of thymocytes was preincubated with 100 μM LiCl before their exposure to DEX, apoptotic cell death induced by DEX was almost completely prevented as determined by both flow cytometric analysis and the terminal deoxynucleotidyltransferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay. DNA laddering assay also documented the inhibition of thymocyte apoptosis by LiCl. Furthermore, we found that the DEX-induced increment of caspase-3 activity in thymocytes was     

The thymic stromal cell line MTSC4 induced thymocyte apoptosis in a non-MHC-restricted manner

Mouse thymic stromal cell line 4 (MTSC4) is one of the stromal cell lines established in our laboratory. While losing the characteristics of epithelial cells, they express some surface markers shared with thymic dendritic cells (TDCs). To further study the biological functions of these cells, we compared the capability of MTSC4 with TDCs in the induction of thymocyte apoptosis, using thymic reaggregation culture system. Apoptosis of thymocytes induced by MTSC4 and TDCs was measured by Annexin V and PI staining and analyzed by flow cytometry. We found that MTSC4 selectively augmented the apoptosis of CD4^ 8^ (DP) thymocytes. This effect was Fas/FasL independent and could not be blocked by antibodies to MHC class I and class II molecules. In addition, MTSC4 enhanced the apoptosis of DP thymocytes from different strains of mice, which implies that MTSC4-induced thymocyte apoptosis is not mediated by the TCR recognition of self peptide/MHC molecules. In contrast to MTSC4, thymocyte apoptosis induced by TDCs was MHC-restricted. Thus, MHC-independent fashion of stromal-DP thymocyte interaction may be one of the ways to induce thymocyte apoptosis in thymus. Our study has also shown that the interaction of MTSC4 stromal cells and thymocytes is required for the induction of thymocyte apoptosis.     

The effects of cell density, attachment substratum and dexamethasone on spontaneous apoptosis of rat hepatocytes in primary culture

Summary The rates of spontaneous cell detachment, cell viability, and apoptosis in primary cultures of rat hepatocytes plated at high and low density were compared. Apoptosis was frequent in detached cells, and the rates of cell detachment and apoptosis were greater in high-density than in low-density cultures. Among attached cells, more cells had condensed or fragmented nuclei in high-density than in low-density cultures. Further, ladder-like DNA fragmentation was not seen in low-cell-density cultures but was clearly evident in high-density cultures. Bax was more highly expressed in cells cultured at high density, and on collagen vs. matrigel, whereas changes of Bcl-2 and Fas expression observed in culture appeared unrelated to the rate of apoptosis. The rate of hepatocyte apoptosis appeared to be identical in low-density cultures on collagen 1 and matrigel, but when cells were cultured at high density, matrigel suppressed apoptosis by more than 50% at 36 h. In hepatocytes cultured on collagen 1, dexamethasone (0.1 μM) suppressed apoptosis in both low- and high-density cultures; higher doses had no further effects. In high density cultures, aurintricarboxylic acid (10 μM) suppressed apoptosis and this improved cell attachment at 48 h. It is concluded that cell viability in primary cultures of rat hepatocytes grown on collagen I is dependent on optimal culture density and that the cell population is regulated, at least in part, by apoptosis. Corticosteroids suppress spontaneous apoptosis of cultured hepatocytes in a non-dose-dependent manner, whereas matrigel abolishes apoptosis induced by increasing cell density. Bax may be an important protein in the cell density and cell matrix-dependent regulation of apoptosis in cultured hepatocytes.     

Transfusion of donor apoptotic splenocytes prolongs cardiac allograft sur-vival in absence of immunosuppression

Although apoptosis has been recently documented to transmit immunosuppressive signals, their significance in allogeneic transplantation has not been reported. In the present study, we investigated the influence of donor apoptotic splenocytes on allograft survival in a SD to Wistar rat cardiac transplant model. Donor splenocytes were isolated and irradiated with ultraviolet (UV) to induce apoptosis in vitro. 5x107 apoptotic, necrotic or untreated donor spleen cells were transfused preoperatively and cardiac allogeneic transplantation     

二龄草鱼脾脏、肝脏组织高表达甘露糖结合凝集素mRNA

Innate immunity is expected to be very important in fish. Mannose-bingding lectin (MBL) participates in the innate immune system as an activator of the complement system and as an opsonin after binding to certain carbohydrate structures on microorganisms. In this experiment, total mRNA was isolated from spleen, liver, gills, thymus, head kidney and kidney of adult and immature grass carp Ctenopharygodon idllus. The cDNA of MBL was obtained by RT-PCR using total mRNA from the spleen of carp as template. Such cDNA was labled with ^32p and used as probe for Northern analysis, and autoradiographic signals were quantified by densitometry analysis. The results showed that MBL was high expressed in the spleen and liver and low in gills, thymus, head kidney and kidney of adult grass carp, and MBL was much lower expressed in spleen and liver of immature grass carp than those of adult grass carp. The results might partially explain why immature grass carp are vulnerable to grass carp hemorrhage virus (GCHV) whereas adult grass carp are not.This suggested that MBL mav be an imoortant anti-GCHV factor [Acta Zoologica Sinica 50 (1): 137 - 140. 2004].     

Clusterin mRNA expression in apoptotic and activated rat thymocytes

Clusterin is a 75-80 kDa heterodimeric glycoprotein,that is produced in most tissues but which exact biological role is still not clear.Pwarticularly,its role in protection or promotion of apoptosis is heavily disputed,since data supporting both views have been reported in several independent sutdies.To clarify this issue,and also to determine whether clusterin expression itself might be affected by apoptosis,in the present study,rat thymocytes were treated with dexamethasone,-a synthetic glucocorticoid that elicits apoptosis in thymocytes-,and clusterin mRNA expression was analyzed by semi-quantitative RT-PCR before and after induction of apoptosis.Interestingly,neither the treatment with dexamethasone in vitro nor triggering of apoptosis in vivo up-regulated clusterin expression,opposing the view that clusterin is involved in apoptotic processes.On the other hand,a new clusterin mRNA isoform was detected and isolated,whose expression ws restricted to freshly isolated thymocytes.This novel isoform lacks the post-translational proteolytic cleavage site and is therefore predicted to encode a monomeric protein.The biological function under normal circumstances,however,will nedd further investigations for clarification.While apoptosis could not modulate clusterin expression,activation of thymocytes with concanavalin A and interleukin-2 resulted in up-regulation of clusterin mRNA level,indicating that clusterin expression is rather under the control of cell activation-mediated rather than apoptosis-induced signals.     

Selective support of a mouse thymus epithelial cell line （MTEC1） to the viability and proliferation of CD4＋CD8—,CD4^—CD8^—,and CD4^＋CD8^＋thymocytes in vitro

The MTEC1 cell line,established in our laboratory,is a normal epithelial cell line derived from thymus medulla of Balb/c mice and these cells constituteively produce multiple cytokines.The selection of thymic microenvironment on developing T cells was investigated in an in vitro system.Unseparated fresh thymocytes from Balb/c mice were cocultured with MTEC1 cells or/and MTEC1-SN,then,the viability,proliferation and phenotypes of cultured thymocytes were assessed.Without any exogenous stimulus,both MTEC1 cells and MTEC1-SN were able to maintain the viability of thymocytes,while only the MTEC1 cells,not the MTEC1-SN,could directly activate thymocytes to exhibit moderate proliferation,indicating that the proliferative signal is delivered through cell surface interatcions of MTEC1 cells and thymocytes.Phenotype analysis on FACS of viable thymocytes after coculture revealed that MTEC1 cells preferentially activate the subsets of CD4^ CD8^-,CD4^ CD^8 and CD^4- CD^8- thymocytes;whereas MTEC1-SN preferentially maintained the viability of CD4^ CD^8- and CD4^-CD8^ thymocyte subsets.For the Con A-activated thymocytes.both MTEC1 cells and MTEC1-SN provided accessory signal(s) to significantly increase the number of viable cells and to markedly enhance the proliferation of thymocytes with virtually equal potency,phenotyped as CD4^ CD8^-,CD4^-CD8^ ,and CD^4-CD8^-subests,In summary,MTEC1 cells displayed Selection of thymic epithelial cells on thymocyte subsets. selective support to the different thymocyte subsets,and the selectivity is dependent on the status of thymocytes.     

Non-neuronal muscarinic receptor activation prevents apoptosis of endothelial cells induced by homocysteine

Objective Endothelial apoptosis plays an important role in the initiation of atherosclerosis. It would be useful to clarify whether activation of non-neuronal muscarinic receptor （NNMR） could prevent endothelial apoptosis and atherosclerosis. We investigated the effects of NNMR activation on regulating rat aortic endothelial cells （RAECs） apoptosis induced by homocysteine, an independent risk factor of atherosclerosis, and further studied its molecular mechanism. Methods RAECs were incubated using homocysteine at the concentration of 2.7 mmol/L for 36 h. RAECs were also pre-treated with carbachol or arecoline to examine their effects. RT-PCR was used to assess changes in the gene expression related to cell apoptosis. Results Incubation of RAECs with homocysteine at the concentration of 2.7 mmol/L resulted in morphologic changes, such as cellular shrinkage, membrane blebbing, chromatin condensation and margination. These could be attenuated by pretreatment with carbachol and arecoline at the concentration of 10 μmol/L for 12 h. Homocysteine induced apoptosis in RAECs and the molecular mechanisms were associated with the regulation of fas, fas-L and caspase-8 in the death receptor pathway, bcl-2, bcl-xL and bax in the mitochondrial pathway, caspase-22 in the endoplasmic reticulum pathway and caspase-3, caspase-6 and p53 as downstream effectors. Carbachol and arecoline attenuated the effects of homocysteine on genes in the death receptor pathway, in the mitochondrial pathway and in the downstream pathway. Atropine could reverse all of the effects of arecoline. Conclusion Activation of NNMR by carbacol and arecoline inhibits homocysteine-induced endothelial cell apoptosis mainly through regulation of death receptor pathway, mitochondrial pathway and downstream effectors.     

Induction of apoptosis and change of bcl—2 expression in macrophage Ana—1 cells by all—trans retinoic acid

Macrophage cells play an important role in the initiation and regulation of the immune response.All-trans retinoic acid (ATRA) and its natural and synthetic analogs (retinoids)affect a large number of biological processes.Recently,retinoids have been shown promise in the therapy and prevention of various cancers.However,many interesting questions related to the activities of retinoids remain to be answered:(I) Molecular mechanisms by which retinoids exert their effects;（Ⅱ)why the clinical uses of retinoids give undesirable side effects of varying severity with a higher frequency of blood system symptoms;(Ⅲ)little is known for its impacts on macrophage cells etc.We set up this experiment,therefore,to examine the apoptosis of ATRA on macrophage Ana-1 cell line.Apoptosis of the cells was quantitated,after staining cells with propidium iodide(PI),by both accounting nuclear condensation and flow cytometry.When the cells were treated with ATRA at or higher than 1μM for more than 24h,significant amount of the apoptotic cells was observed.Induction of apoptosis of Ana-1 cells by ATRA was in time-and dose-dependent manners,exhibiting the similar pattern as the apoptosis induced by actinomycin D (ACTD).ATRA treatment of Ana-1 cells also caused the changes of the mRNA levels of apoptosis-associated gene bcl-2,as detected by Northern blot analysis.The temporal changes of bcl-2 expression by ATRA was also parallel to that by ACTD.In conclusion,ATRA can induce apoptosis in macrophage cells,which may be helpful in understanding of immunological functions retinoids.     

Increased leptin by hypoxic-preconditioning promotes autophagy of mesenchymal stem cells and protects them from apoptosis

Autophagy is the basic catabolic progress involved in cell degradation of unnecessary or dysfunctional cellular components.It has been proven that autophagy could be utilized for cell survival under stresses.Hypoxic-preconditioning(HPC)could reduce apoptosis induced by ischemia and hypoxia/serum deprivation(H/SD)in bone marrow-derived mesenchymal stem cells(BMSCs).Previous studies have shown that both leptin signaling and autophagy activation were involved in the protection against apoptosis induced by various stress,including ischemia-reperfusion.However,it has never been fully understood how leptin was involved in the protective effects conferred by autophagy.In the present study,we demonstrated that HPC can induce autophagy in BMSCs by increased LC3-II/LC3-I ratio and autophagosome formation.Interestingly,similar effects were also observed when BMSCs were pretreated with rapamycin.The beneficial effects offered by HPC were absent when BMSCs were incubated with autophagy inhibitor,3-methyladenine(3-MA).In addition,down-regulated leptin expression by leptin-shRNA also attenuated HPC-induced autophagy in BMSCs,which in turn was associated with increased apoptosis after exposed to sustained H/SD.Furthermore,increased AMP-activated protein kinase phosphorylation and decreased mammalian target of rapamycin phosphorylation that were observed in HPC-treated BMSCs can also be attenuated by down-regulation of leptin expression.Our data suggests that leptin has impact on HPC-induced autophagy in BMSCs which confers protection against apoptosis under H/SD,possibly through modulating both AMPK and mTOR pathway.     

The effects of corticosteroid hormones and thyroid hormones on lymphocyte viability and proliferation during development and metamorphosis of Xenopus laevis

Abstract. Metamorphosis in the South African clawed frog, Xenopus laevis , is characterized by a striking loss of lymphocytes in the thymus, liver, and spleen. Changes in the proliferative responses of splenocytes and thymocytes to T cell mitogens and semi-allogeneic cells are also observed at metamorphosis. Because the levels of circulating thyroid hormones (TH) and corticosteroid hormones (CH) increase dramatically during the climax of metamorphosis, we have investigated the possible role of TH and CH as mediators of the changes in lymphocyte numbers or lymphocyte function. Here we report on the in vitro effects of CH and TH on lymphocyte viability and on phytohemagglutinin-P (PHA)-stimulated lymphocyte proliferation at prometamorphosis and climax of metamorphosis. We have observed consistently significant inhibition of proliferation by corticosterone. In contrast, we have observed inconsistent inhibition of proliferation by both thyroxine (T₄) and triiodothyronine (T₃). In short-term studies, the viability of thymocytes and splenocytes was reduced in the presence of CH but not TH.
These observations are consistent with a hypothesis that loss of larval lymphocytes and changes of lymphocyte function at metamorphosis may be due to elevated concentrations of CH rather than TH.
Because CH have been shown to enhance TH-induced effects during metamorphosis, we looked at the combined effects of these agents on PHA-stimulated lymphocyte proliferation. While each agent was inhibitory in several experiments, there was no significantly greater inhibition when splenic lymphocytes were cultured with both.     

Identification of the avian homologues of mammalian CD4 and CD8 antigens

Two mAb were produced against chicken T cells. The CT4 antibody precipitated a polypeptide of Mr 64,000 under both reducing and non-reducing conditions. The CT8 antibody precipitated a molecule of Mr 63,000 under non-reducing conditions and polypeptide chains of Mr 34,000 under reducing conditions, suggesting that the CT8 molecule is a disulfide-linked homodimer. Tissue distribution studies by immunofluorescence revealed that the CT4 and CT8 Ag were expressed by the majority of thymocytes and by subpopulations of CT3+ cells in peripheral tissues. The CT4 reactive molecule was found on approximately 70% of thymocytes, 10% splenocytes, and 45% of lymphoid cells in blood. The CT8 reactive molecule was expressed on approximately 80% of thymocytes, 50% of spleen cells, and 15% of blood lymphocytes. Two-color immunofluorescence indicated that the CT4 and CT8 Ag were expressed together on most thymocytes and on mutually exclusive subsets of cells in the spleen and blood. Ontogenic studies revealed a sharp increase in the frequencies of CT4+ and CT8+ cells in the thymus between days 13 and 16 embryonic life. Both CT4 and CT8 antibodies inhibited PHA- and Con A-induced proliferative responses of splenocytes, and the degree of inhibition correlated with the frequencies of CT4+ and CT8+ lymphoblasts. Treatment of spleen cells with CT4 antibody and inhibited PWM-induced IL-2 production, and removal of CT8+ cells inhibited the cytolytic activity induced by allogeneic lymphocyte stimulation. Macrophages did not express detectable CT4 reactivity. These results suggest that the CD4 and CD8 molecules and their tissue-restricted patterns of expression are highly conserved in birds and mammals.     

T cell induction of precursor B cells: Temporal separation of helper T cell functional activities

Summary The temporal relationships involved in T cell induction of immunoglobulin-secreting B cells have been studied by employing a pulse label technique, in vitro. It was shown that addition of rabbit thymocytes or splenic T cells to B cell-enriched splenocyte populations at the time of initiation of cultures resulted in a marked enhancement in induction of immunoglobulin-secreting cells. However, even a two-hour delay in the addition of thymus cells was sufficient to reduce substantially the extent of induction when measured 70 hours later. Besides this early requirement for thymocytes, a late requirement was also detectable. Thus, thymus cells and splenocyte populations upon being mixed, subsequent to being cultured separately for 72 hours, yielded a several-fold enhancement in [³H]-immunoglobulin secreted during the course of a 90-minute labeling period with [³H]-leucine. Moreover, both the early and late thymocyte effects were lost after treatment with anti-thymocyte serum and complement.The thymocyte-mediated enhancement of immunoglobulin secretion by splenocytes that occurs late in the induction process was detected with spleen cells cultured for two or three days but not with freshly-isolated splenocytes. Although the rate of appearance of extracellular immunoglobulins was markedly enhanced by fresh thymus cells, the rate of appearance of intracellular immunoglobulins in such spleen cells was unchanged. The secretion-stimulating (secretagogue) activity of thymocytes appeared to be specific in that thymus cells were without effect on the rate of secretion of serum albumin by liver cells.In regard to the induction of immunoglobulin-secreting cells, both B and T cell-enriched population's were sensitive to mitomycin C treatment performed before initiation of cell culture, indicating that not only B cells but also T cells undergo some form of differentiation or maturation prior to functioning in the induction of immunoglobulin-producing cells. It should be noted in this context that the late T cell requirement was unaffected by prior mitomycin C treatment of thymocytes. On the other hand, thymocytes heated at 60°C for 5 minutes did not enhance immunoglobulin secretion when added at any time and the late thymocyte requirement could not be replaced with medium in which thymocytes had been previously cultured.     

Immunomodulations of thymocytes and splenocytes in trained rats.

The aim of this study was to describe the effects of training (running) on thymus and spleen cells in the rat. Young Wistar control rats (n = 6), rats trained for 4 wk (n = 5), and rats trained for 4 wk followed by 1 wk of intensive training (3 h/day, n = 6) were studied. Various lymphocyte surface and nuclear markers were determined by immunocytochemistry. The results show that 4 wk of training 1) decreased the percentage of bromodeoxyuridine (BrdU+) thymocytes (cell in phase S of the cycle, immature thymocytes; P less than 0.05) and the viability of thymocytes stimulated with concanavalin A (Con A; P less than 0.05) and 2) increased the absolute number of CD8+ (suppressor/cytotoxic T cells; 29%) and the percentage of CD8+ splenocytes (P less than 0.01). An additional week of intensive training in the 4-wk trained rats induced 1) a decrease in the absolute number of thymocytes (25%, P less than 0.05), TCR+ thymocytes, splenocytes (28%, P less than 0.01), T, CD4+ (helper T cells; 34%), and CD8+ (31%) splenocytes (P less than 0.01) and 2) an increase in the viability of splenocytes after stimulation with Con A for 72 h (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Splenocytes incorporated with exogenous gangliosides induce a mixed lymphocyte reaction in autologous lymphocytes

SWR splenocytes incorporated with mixed gangliosides triggered an efficient mixed lymphocyte reaction in autologous thymus lymphocytes. The potency of the ganglioside-incorporated splenocytes as stimulators in the autologous system was eight to ninefold greater than background effect of untreated splenocytes. The induced mixed lymphocyte reaction was not due to free gangliosides in culture medium and occurred only if the gangliosides were incorporated into the triggering splenocytes, but not into the responding thymocytes. The mixed lymphocyte reaction generated by gangliosides incorporation in the autologous system is similar to that reaction in the allogeneic system with regard to the time course of [³H]thymidine incorporation.     

Production and characterization of monoclonal antibodies to rabbit lymphocyte subpopulations. I. Tissue immunofluorescence and flow cytometric analysis

Nine monoclonal antibodies to rabbit T cells and B subpopulations have been generated from three separate fusions of spleen cells from mice immunized with fractionated populations of rabbit lymphocytes. These monoclonal antibodies, as well as a previously described rabbit T cell monoclonal antibody, 9AE10, have been analyzed by immunofluorescence staining on frozen tissue sections of rabbit thymus, spleen, and appendix. This screening method permits rapid identification of the lymphocyte subdomains in each tissue which is not possible by other screening methods. Each monoclonal antibody selected has a unique tissue staining pattern. Flow cytometric analysis of these monoclonal antibodies, using indirect immunofluorescence techniques on thymocytes, splenocytes, and PBL, revealed varying percentages of positive cells and individual mean fluorescence intensities indicating different epitope densities for each antigen. These monoclonal antibodies are now being used to characterize normal lymphocyte function and the role of specific lymphocyte subpopulations in experimental disease models in the rabbit.     

Chronic metoclopramide treatment stimulates T lymphocyte proliferation in the spleen but not in the thymus.

The effect of chronic metoclopramide administration (for 10 days at a daily dose of 5 mg/kg body weight subcutaneously) on cell proliferation in spleen and in thymus was investigated. Cell proliferation was evaluated by the stathmokinetic method with the use of vincristine. It was found that metoclopramide administration results in a statistically significant increase in the value of the mean mitotic activity rate index (MMAR) of splenocytes in the areas around arteries. At the same time no statistically significant changes were demonstrated in the MMAR index values obtained for splenocytes present in the germinal centers of the spleen. No significant changes in the MMAR index could also be found for thymocytes.     

Functional activity of T and B lymphocytes of mice undergoing spontaneous loss of tolerance]

The functional activity of splenocytes and thymocytes of mice tolerant to sheep red blood cells was investigated one and four weeks after tolerance induction. The tolerance was achieved by cyclophosphamide. The immunocompetence of thymocytes was fully reversed in lfour week time. The functional activity of T and B lymphocytes of the spleen was also partially recovered four weeks after tolerance induction. Preliminary thymectomy weakened but did not prevent completely the immunocompetence of T cells of the spleen from being recovered. No Tsuppressants were found in the thymus or spleen of the tolerant animals.     

Release of immature cells from the thymus during solid tumor growth: identification by assay of TdT activity.

In vivo anti-tumor activity of spleen cells from C3H/eb mice bearing a syngeneic fibrosarcoma was shown previously to decline to an undetectable level and be replaced by tumor-enhancing activity as tumor growth proceeds. In the light of our findings that thymocytes in the early stages of thymic processing can bring about tumor enhancement, we postulated that premature release of thymocytes and their accumulation in the spleen might account for the loss of the anti-tumor response. In the present experiments an injection of thymocytes did in fact cancel the anti-tumor response of reactive splenocytes from tumor-bearing mice. In order to determine whether premature thymocyte release occurs naturally in the tumor-bearing animals, we assayed activity of the enzyme TdT (as a marker for thymus cells) in the spleens of these mice during progressive tumor growth. Cells with TdT activity were clearly evident in the spleens of the tumor-bearing animals, were derived from the thymus, and accumulated in parallel to the loss of anti-tumour reactivity.     

高原低氧免疫损伤及其干预措施的研究

目的:探讨高原低氧损伤免疫系统的特征及其可能机制,研究高原低氧免疫损伤的干预措施。方法:测定低氧暴露不同时间小鼠免疫器官指数、外周血和免疫器官T淋巴细胞亚群的变化;观察小鼠免疫器官淋巴细胞凋亡率及小鼠肺脏和肾脏病理学改变。采用预防给药方式,研究中药组方对低氧免疫损伤小鼠的干预作用。结果:①模拟海拔8000m低氧暴露8h后,小鼠胸腺CD4+CD8+细胞数显著下降,CD4+CD8-、CD4-CD8+细胞数显著增加(P0.01);低氧暴露3d后,外周血CD4+细胞明显减少(P0.05),CD4+/CD8+比值显著降低(P0.05),胸腺CD4+CD8+细胞数进一步下降,CD4+CD8-、CD4-CD8+细胞数进一步增加,小鼠脾脏、胸腺淋巴细胞晚期凋亡和坏死率均显著增加(P0.05);低氧暴露6d后,小鼠脾指数显著性增加(P0.01);胸腺指数显著性降低(P0.01),脾CD4+、CD8+细胞数显著降低(P0.01),脾脏和胸腺淋巴细胞晚期凋亡率和坏死率进一步增加(P0.01),活细胞率显著降低(P0.01),脾脏淋巴细胞早期凋亡率显著增加(P0.01)。整个低氧暴露过程中外周血CD8+无显著性变化。②新复方党参、香杞多糖、二者联合应用均能显著增加低氧免疫损伤小鼠外周血CD3+、CD4+、脾脏CD4+的细胞水平(P0.01,P0.05),对脾脏CD8+细胞水平没有显著影响。香杞多糖及其与新复方党参联合应用均能进一步降低胸腺CD4+CD8+,进一步增加CD4+CD8-的细胞水平(P0.01),未见对CD4-CD8+细胞水平的影响;新复方党参对低氧免疫损伤小鼠胸腺没有显著性影响。结论:模拟海拔8000m低氧暴露后小鼠外周发挥免疫作用的淋巴细胞数减少可能与低氧暴露早期淋巴细胞凋亡率和坏死率增加和肺脏淋巴细胞分布增多有关。新复方党参和香杞多糖作为低氧免疫损伤干预措施,具有一定发展前景。