Dihydroquercetin Ameliorates LPS-induced Neuroinflammation Thiab Memory Deficit Ⅱ

3. Cov txiaj ntsig

3.1. DHQ ameliorated LPS-induced alterations nyob rau hauv spatial recognition nco tus cwj pwm kuaj nyob rau hauv lub Y-maze xeem

Peb tau ua qhov kev paub txog kev paub txog kev nco tus cwj pwm hauv Y-maze los ntsuas qhov cuam tshuam ntawm DHQ ntawm LPS-vim tus cwj pwm tsis nco qab. Kev txheeb xyuas kev txheeb xyuas siv ob txoj kev ANOVA qhia qhov sib txawv tseem ceeb hauv feem pua ​​​​ntawm caj npab nkag hauv kev sim-1 thiab kev sim-2 ntawm pawg [F (4, 80) ¼ 2.23, p < {{15 } }.

Nyem rau Rou cong rong kom nco txhim kho

Kev soj ntsuam ntxiv uas siv qhov kev xeem tom qab hoc pom qhov poob tseem ceeb hauv kev paub txog kev nco txog tus cwj pwm nrog LPS kev tswj hwm piv rau cov nas tswj. Muaj qhov sib txawv tseem ceeb ntawm kev tswj hwm, LPS, DHQ0.5, thiab 1 ug / kg pawg. Kev kho mob nrog 2 ug / kg attenuated LPSinduced poob ntawm spatial recognition nco. Txawm li cas los xij, DHQ-0.5 thiab DHQ-1 ug/kg tsis tau qhia tias muaj kev hloov pauv rau LPS-induced poob nyob rau hauv lub spatial recognition nco. Nws muaj nyob rau hauv daim duab 2(a).

3.2. DHQ txhim kho LPS-vim kev hloov pauv hauv kev xav paub tus cwj pwm hauv kev sim Ymaze

Peb tshawb xyuas qhov cuam tshuam ntawm DHQ ntawm kev xav paub tus cwj pwm nyob rau hnub {{{0}} raws li tau piav qhia hauv daim duab 2(b) hauv qab no. Peb pom qhov sib txawv tseem ceeb hauv kev sim-1 thiab kev sim-2 ntawm pawg [F (4, 80) ¼ 1.77, p < 0.05], caj npab [F ( 1, 80) ¼ 83.9, p < 0.05] thiab kev cuam tshuam tseem ceeb ntawm pawg thiab caj npab [F (4, 50) ¼ 99.7, p < 0.05] thaum soj ntsuam nrog ob txoj kev ANOVA.

Qhov kev sim tom qab hoc tau qhia tias tus cwj pwm xav paub tau txo qis nrog LPS kev tswj hwm piv rau cov nas tswj. Kev kho mob ntawm DHQ-2 ug/kg ua rau txo qis LPS vim qhov xav paub txog tus cwj pwm. Txawm li cas los xij, DHQ-0.5 ug / kg tsis ua rau muaj kev hloov pauv rau LPSinduced txo qis hauv kev xav paub tus cwj pwm. Cov txiaj ntsig ntawm DHQ-2 ug/kg tau pom tias yog qhov tseem ceeb tshaj DHQ-1 ug/kg hauv kev txhim kho LPS-vim txo qis hauv kev xav paub.

3.3. DHQ txhim kho kev ua haujlwm nco hauv Y-maze xeem

Cov txiaj ntsig ntawm DHQ ntawm kev puas tsuaj ntawm qhov chaw nco nyob rau hnub {{{0}}} tom qab LPS txhaj tshuaj hauv Y-maze xeem tau piav qhia hauv daim duab 2(c) hauv qab no. Kev txheeb xyuas kev txheeb xyuas siv ib-txoj kev ANOVA tau pom tias muaj qhov sib txawv tseem ceeb hauv kev hloov pauv tus cwj pwm hauv Y-maze test paradigm ntawm cov pab pawg [F (4, 40) ¼ 128, p <0.05]. Qhov kev sim tom qab-hoc tau qhia tias tus cwj pwm hloov pauv hloov pauv tau txo qis nrog LPS kev tswj hwm piv rau cov nas tswj.

Qhov sib txawv tseem ceeb kuj tau pom ntawm kev tswj hwm thiab DHQ 0.5 thiab 1 ug / kg pawg. Kev kho mob ntawm DHQ ntawm 1 ug / kg thiab 2 ug / kg attenuated LPS-vim txo qis hauv kev hloov pauv tus cwj pwm, uas qhia txog kev nce hauv kev ua haujlwm nco. Cov txiaj ntsig ntawm DHQ-2 ug/kg tau pom tias tseem ceeb dua DHQ-1 ug/kg, hos DHQ-0.5 ug/kg tsis ua rau muaj kev hloov pauv rau LPS- induced txo qis hauv kev ua haujlwm nco.

3.4. DHQ mitigated LPS-induced alterations in transfer latency (TL) hauv EPM cwj pwm

Txhawm rau ntsuas qhov kev nco mus ntev, peb tau kawm txog qhov cuam tshuam ntawm DHQ ntawm kev hloov latency nyob rau hnub-9 thiab hnub-10 tom qab LPS txhaj tshuaj hauv EPM kuaj raws li tau piav qhia hauv daim duab 3(a) hauv qab no. Kev txheeb cais siv ob txoj kev ANOVA qhia qhov sib txawv tseem ceeb hauv kev sim-1 thiab kev sim-2 ntawm cov pab pawg [F (4, 80) ¼ 403.1, P < 0.00 .05], sij hawm [F (1, 80) ¼ 781.4, p< 0.05] and a significant interaction between groups and time [F (4, 80) ¼ 15.11, p < 0.05]. 

Qhov kev sim tom qab hoc tau qhia tias LPS txhaj tshuaj tau nce TL piv rau cov nas tswj. Cov ntaub ntawv qhia tau hais tias TL ntawm pawg tswj hwm tau txawv ntawm tag nrho lwm pawg nyob rau hnub-10 tab sis nyob rau hnub-9, TL ntawm pawg tswj tau txawv ntawm LPS, DHQ{{3} }.5, thiab 1 ug / kg nkaus xwb. DHQ-0.5 ug/kg tsis ua rau muaj kev hloov pauv rau LPS-induced nce hauv TL. Txawm li cas los xij, LPS-induced nce hauv TL tau txo qis nrog DHQ-1 ug/kg thiab DHQ-2 ug/kg.

3.5. DHQ nce kev qhib caj npab nkag hauv EPM tus cwj pwm kuaj

Kev ntxhov siab tus cwj pwm yog tshwm sim hauv cov nas los ntawm induction ntawm LPS. Qhov cuam tshuam ntawm DHQ ntawm qhov feem pua ​​​​ntawm kev qhib caj npab nkag rau hnub {{{0}}} tom qab txhaj tshuaj LPS hauv EPM tau piav qhia hauv daim duab 3(b) hauv qab no. Ib-txoj kev ANOVA tau pom qhov sib txawv tseem ceeb hauv feem pua ​​​​qhib caj npab nkag ntawm pawg [F (4, 40) ¼ 101, p < 0.05].

Qhov kev sim tom qab-hoc tau tshaj tawm tias LPS txhaj tshuaj txo qis feem pua ​​​​ntawm kev qhib caj npab piv rau cov nas tswj. Cov ntaub ntawv tau qhia tias muaj qhov sib txawv tseem ceeb ntawm kev tswj hwm thiab txhua pab pawg. DHQ-0.5 ug/kg tsis ua rau muaj kev hloov pauv rau LPS-vim txo qis hauv feem pua ​​​​ntawm cov khoom qhib-caj npab. Txawm li cas los xij, LPS ua rau txo qis hauv feem pua ​​​​ntawm kev qhib caj npab nkag tau zoo nrog DHQ-1 ug/kg thiab DHQ-2 ug/kg tswj hwm.

3.6. DHQ txo qis LPS-vim kev hloov pauv hauv lub sijhawm qhib caj npab siv hauv EPM tus cwj pwm kuaj

Kev txheeb xyuas cov ntaub ntawv coj tus cwj pwm siv ib-txoj kev ANOVA qhia qhov sib txawv tseem ceeb hauv lub sijhawm qhib-arm siv ntawm pawg [F (4, 40) ¼ 292.2, p< 0.05]. The post-hoc test revealed that LPS injection significantly decreased the percentage of open-arm time spent compared to control rats. Statistical data also showed that time spent in the open arm by the control group was significantly different from all other groups. DHQ-0.5 μg/kg caused a significant change to the LPS-induced decrease in the open arm time spent. However, the LPS induced a decrease in the open arm time spent significantly improved with DHQ-1 μg/kg and DHQ-2 μg/kg even more significant than DHQ-0.5 μg/kg. It is shown in Fig. 3(c).

3.7. DHQ tsis pom muaj qhov cuam tshuam rau tag nrho cov caj npab nkag hauv EPM tus cwj pwm kuaj

Cov txiaj ntsig ntawm DHQ ntawm tag nrho cov caj npab nkag rau hnub{{0}} tom qab txhaj tshuaj LPS hauv EPM tau piav qhia hauv daim duab 3(d) hauv qab no. Kev txheeb xyuas kev txheeb xyuas siv ib-txoj kev ANOVA tau pom tias tsis muaj qhov sib txawv tseem ceeb hauv tag nrho cov caj npab nkag ntawm pawg [F (4, 40) ¼ 0.894, p < 0.05]. Qhov kev sim tom qab-hoc tau qhia tias LPS txhaj tshuaj tsis ua rau muaj kev hloov pauv tseem ceeb hauv tag nrho cov caj npab nkag ntawm cov pab pawg. Tsis muaj qhov koob tshuaj DHQ ua rau muaj kev hloov pauv tseem ceeb hauv tag nrho cov caj npab nkag.

3.8. DHQ koob tshuaj-raws li txo LPS-vim kev hloov pauv hauv lub sijhawm tsis muaj zog hauv EPM tus cwj pwm

Cov txiaj ntsig ntawm DHQ ntawm lub sijhawm tsis tuaj yeem nyob rau hnub{{0}} tom qab txhaj tshuaj LPS hauv EPM tau piav qhia hauv daim duab 3(e) hauv qab no. Ib txoj kev ANOVA qhia qhov sib txawv tseem ceeb hauv lub sijhawm tsis muaj zog ntawm cov pab pawg [F (4, 40) ¼ 138.3, p < 0.05]. Qhov kev sim tom qab hoc tau pom tias LPS txhaj tshuaj tau nce lub sijhawm tsis muaj zog piv rau cov nas tswj. DHQ0.5 tau pom tias tsis muaj kev hloov pauv hauv LPS-induced nce nyob rau hauv lub sij hawm immobility.

Lub sijhawm immobility hauv pawg tswj tau tsawg dua LPS thiab DHQ -0.5 thiab 1 ug / kg. Txawm li cas los xij, LPS-induced nce nyob rau hauv lub sij hawm immobility tau txo qis nrog DHQ-1 ug/kg thiab DHQ-2 ug/kg, DHQ-2 ug/kg txo lub sij hawm immobility ntau dua. tshaj DHQ-1 ug/kg.

3.9. DHQ txhim kho txhais tau tias cov ntshav ntws mus rau hauv lub hlwb hloov los ntawm LPS induction

Cov txiaj ntsig ntawm DHQ ntawm qhov txhais tau tias cov ntshav ntws hauv hlwb tau raug soj ntsuam nyob rau hnub 10 tom qab LPS txhaj tshuaj siv lub laser Doppler imager tau piav qhia hauv daim duab 4 hauv qab Kev Tshawb Fawb Kev Tshawb Fawb siv ib-txoj kev ANOVA qhia qhov sib txawv tseem ceeb ntawm pawg [F (4 , 25) ¼ 41.9, p < 0.05]. Qhov kev sim tom qab-hoc tau qhia tias LPS txhaj tshuaj coj qhov txo qis hauv cov ntshav ntws mus rau hauv lub hlwb piv rau kev tswj cov nas.

Cov ntshav ntws hauv cov nas tswj kuj tseem sib txawv thaum piv rau DHQ -0.5 thiab 1 ug / kg. Txawm li cas los xij, DHQ-0.5 ug/kg thiab DHQ-1 ug/kg tsis ua rau muaj kev hloov pauv rau LPS-vim txo qis hauv cov ntshav ntws. Txawm li cas los xij, LPS-induced poob nyob rau hauv qhov txhais tau tias cov ntshav ntws tau zoo tuaj nrog DHQ-2 ug/kg.

3.10. DHQ rov qab qib ntawm acetylcholine hloov los ntawm LPS induction

Acetylcholine yog ib qho ntawm cov neurotransmitters tseem ceeb hauv lub hlwb koom nrog kev kawm thiab kev nco (Myhrer, 2003). Cov nyhuv ntawm DHQ ntawm LPS-induced alterations nyob rau hauv cov theem ntawm acetylcholine yog depicted nyob rau hauv daim duab 5(a) hauv qab no. Ib-txoj kev ANOVA tau pom qhov sib txawv ntawm qhov sib txawv ntawm acetylcholine ntawm cov pab pawg [F (4, 10) ¼ 337, p < 0.05].

Qhov kev sim tom qab hoc qhia tau tias LPS txhaj tshuaj txo qis acetylcholine hauv thaj av hippocampus piv rau pawg tswj hwm. DHQ-0.5 ug/kg tsis ua rau muaj kev hloov pauv loj rau LPS-vim txo qis hauv acetylcholine concentration. Txawm li cas los xij, LPS-vim txo qis hauv acetylcholine concentration tau nce nrog DHQ-1 ug/kg thiab DHQ-2 ug/kg. Txawm li cas los xij, DHQ-2 ug/kg nruab nrab nce siab hauv acetylcholine concentration yog qhov tseem ceeb tshaj DHQ-1 ug/kg.

3.11. Cov nyhuv ntawm DHQ ntawm LPS-vim kev hloov pauv hauv acetylcholine-esterase kev ua haujlwm

Cov txiaj ntsig ntawm DHQ ntawm LPS-vim kev hloov pauv hauv AchE kev ua tom qab LPS txhaj tshuaj tau piav qhia hauv daim duab 5(b) hauv qab no. Ib-txoj kev ANOVA qhia qhov sib txawv tseem ceeb hauv AchE kev ua ntawm cov pab pawg [F (4, 10) ¼ 482, p< 0.05]. It was further proved by the post-hoc test that LPS injection significantly increased the AchE activity compared to the control group rats.

Cov ntaub ntawv tau nthuav tawm ntxiv tias AchE kev ua haujlwm ntawm pawg tswj hwm kuj tseem tsawg dua li txhua pab pawg. DHQ-0.5 ug/kg tsis ua rau muaj kev hloov pauv loj rau LPS-induced nce hauv AchE kev ua. Txawm li cas los xij, LPS ua rau muaj kev nce ntxiv hauv AchE kev ua ub no kom txo qis nrog DHQ-1 ug/kg thiab DHQ-2 ug/kg. DHQ-2 ug/kg txo qis hauv cov haujlwm AchE yog qhov tseem ceeb tshaj DHQ-1 ug/kg.

3.12. DHQ txo qis pro-inflammatory IL-6 hauv LPS-induced tsiaj

Peb tau kawm txog cov txiaj ntsig ntawm DHQ ntawm qhov mob cytokine IL {{0}} tom qab LPS induction raws li tau piav qhia hauv daim duab 6 hauv qab no. Kev txheeb xyuas txheeb cais qhia qhov sib txawv tseem ceeb hauv qhov concentration ntawm IL-6 hauv ntau pawg. Muaj qhov sib txawv tseem ceeb ntawm cov pab pawg [F (4, 10) ¼ 3016, p < 0.05] as per one-way ANOVA.

Qhov kev xeem tom qab hoc qhia tias LPS txhaj tshuaj ua rau muaj kev nce qib ntawm IL-6 piv rau cov nas tswj. IL-6 concentration yog qhov sib txawv ntawm cov pab pawg raws li piv nrog pawg tswj hwm. DHQ-0.5, 1, thiab 2 ug/kg tau pom qhov hloov pauv loj rau LPS-induced nce hauv qib IL-6. Txawm li cas los xij, DHQ-2 ug/kg kho kom txo qis hauv qib IL-6 yog qhov tseem ceeb tshaj plaws thaum piv rau lwm ob koob tshuaj. DHQ-1 ug/kg tau pom tias tseem ceeb dua DHQ-0.5 ug/kg.

3.13. DHQ qhia txog kev ua haujlwm antioxidant

Peb kuj tau tshawb xyuas cov khoom antioxidant ntawm DHQ. Daim duab 7 qhia txog cov txiaj ntsig ntawm DHQ ntawm cov enzymes antioxidant thaum LPS induction. Oneway ANOVA qhia qhov sib txawv tseem ceeb ntawm pawg [F (4,10) ¼ 186.7, p < 0.05], MDA [F (4, 10) ¼ 47.40, p <0.05], thiab NO [F (4, 10) ¼ 18.76, P < 0.05] qib.

Qhov kev sim tom qab-hoc tau qhia tias LPS txhaj tshuaj txo qis CAT kev ua haujlwm thiab nce LPO kev ua haujlwm, thiab nce NO qib raws li piv nrog pawg tswj hwm. Kev ua CAT tau txhawb nqa tau zoo nrog DHQ-2 ug/kg tswj hwm. Ntxiv mus, LPO kev ua haujlwm tau txo qis nrog DHQ-0.5, 1, thiab 2 ug / kg. DHQ-1 thiab 2 ug / kg tab sis tsis yog DHQ-0.5 ug / kg kev tswj hwm txo qis tsis muaj kev ua haujlwm loj thaum piv nrog LPS pawg.

4. Kev sib tham

Qhov tseem ceeb ntawm txoj kev tshawb no yog tias DHQ tau pom ntau lub tswv yim ntawm kev ua haujlwm los ntawm kev txo qis LPS-induced neuroinflammation thiab kev txawj ntse tsis txaus. Kev sib raug zoo ntawm neuroinflammation thiab kev kawm thiab kev nco tau zoo tsim los ntawm kev tshawb fawb txog kev kho mob thiab kev kho mob (Liu li al., 2012). Y-maze yog ib qho ntawm feem ntau siv mazes los ntsuas kev kawm thiab kev nco hauv cov qauv tsiaj.

Qhov kev hloov pauv tus cwj pwm tsis zoo yog qhov qhia txog kev ua haujlwm rov qab ua haujlwm nco hauv Y-Maze xeem (Onaolapo li al., 2012). LPS txo qis kev hloov pauv tus cwj pwm hauv Y-Maze qhov kev sim qhia txog qhov tsis txaus ntawm kev ua haujlwm nco.

Raws li pom hauv daim duab 2 (c) DHQ-1 thiab 2 ug/kg txo qis LPS-induced poob hauv kev ua haujlwm nco. Nws kuj tau pom tias DHQ-1 thiab 2 ug / kg attenuated LPS induced ib tug txo nyob rau hauv lub tshiab caj npab thiab ib tug nce nyob rau hauv paub caj npab nkag raws li nyob rau hauv daim duab 2 (b). Yog li ntawd, nws txhim kho spatial recognition nco.

Txoj kev tshawb fawb Y-maze kuj tau pom tias muaj kev txhim kho tseem ceeb hauv qhov chaw nco nrog DHQ-2 ug/kg tom qab LPS txhaj tshuaj raws li qhia hauv daim duab 2 a. Kev tswj hwm ntawm DHQ tau pom tias yuav txhim kho spatial nco nyob rau hauv oligomeric-A -kho nas qauv (Wang li al., 2018).

Cov kev tshawb fawb yav dhau los (Frühauf-Perez li al., 2018) tau qhia tias LPS txhaj tshuaj cuam tshuam kev nco mus ntev. Raws li pom hauv daim duab 3 (a), DHQ hauv koob tshuaj 1 thiab 2 ug / kg kho tau txhim kho lub cim xeeb ntev hauv TL kev coj cwj pwm. Raws li piv rau hnub-9, TL hnub-10 pom qhov txo qis; qhov no qhia txog kev txhim kho hauv kev nco mus ntev. Ib txoj kev tshawb fawb ua ntej (Swiergiel thiab Dunn, 2007) tau qhia tias LPS txhaj tshuaj ua rau muaj kev ntxhov siab zoo li tus cwj pwm vim nws ua rau txo qis ntawm feem pua ​​​​ntawm kev nkag thiab lub sij hawm siv rau hauv qhov qhib caj npab hauv EPM txoj kev kawm.

Hauv peb txoj kev tshawb fawb, DHQ tau txhim kho kev ntxhov siab zoo li tus cwj pwm raws li daim duab 3 (c). LPS infusion tsis pom muaj kev cuam tshuam rau lub locomotor kev ua si ntawm cov tsiaj sim raws li cov ntaub ntawv ntawm caj npab tag nrho, uas qhia tau hais tias lub cev muaj zog tsis muaj kev cuam tshuam li hauv daim duab 3 (c). Neuroinflammation txo cerebral txhais tau tias ntshav ntws (CBF) thiab induces cellular kev nyuaj siab, uas yuav pab tau rau kev txawj ntse tsis xws luag (Zlokovic, 2005).

Nws cov txheej txheem yuav cuam tshuam txog kev ua haujlwm tsis zoo ntawm cov hlab ntsha neurovascular uas ua rau muaj kev cuam tshuam tsis zoo ntawm cov neurotoxic molecules los ntawm lub hlwb mus rau cov ntshav thiab qhov tsis sib xws ntawm lub zog metabolism thiab khoom noj khoom haus (Zlokovic, 2008). Nyob rau hauv txoj kev tshawb no, LPS txhaj tshuaj txo qhov txhais tau tias CBF thiab qhov txo qis hauv qhov txhais tau tias CBF tau txhim kho tau zoo nrog DHQ-2 ug/kg, qhia txog nws cov tshuaj tiv thaiv neuroinflammatory raws li qhia hauv daim duab 4.

Cov kab mob cholinergic muaj lub luag haujlwm tseem ceeb hauv kev nco, thiab nws qhov kev tsis txaus ntseeg tau koom nrog hauv cov kab mob neuroinflammation (Nizri li al., 2006). Nws tau raug pom tias LPS induction ua rau muaj kev nce hauv AChE kev ua haujlwm. Yog li, AChE inhibitors tau raug tshaj tawm rau ameliorate neuroinflammation-induced neurodegeneration (Nizri li al., 2006). Hauv txoj kev tshawb no, LPS induction ua rau muaj kev poob qis hauv qib Ach raws li qhia hauv daim duab 5 (a). thiab ib qho ntxiv hauv AChE cov dej num (Fig. 5 (b)). hauv hippocampus.

Cov txiaj ntsig pom tau tuaj yeem yog vim muaj cov kab mob neuroinflammation-induced neurodegeneration ntawm cholinergic neurons hauv hippocampus (Kalb li al., 2013). DHQ-1 thiab 2 ug/kg thim rov qab cov kev hloov pauv los ntawm LPS infusion hauv ACh qib thiab AChE kev ua raws li qhia hauv Fig.5 (a) thiab Fig.5 (b) raws li. Cov ntaub ntawv no qhia tias DHQ tuaj yeem muaj txiaj ntsig zoo rau cholinergic system hauv cov qauv neuroinflammation ntawm LPS.

Qhov tsis sib xws ntawm ROS ntau lawm thiab tshem tawm hauv cov kab mob lom neeg ua rau muaj kev ntxhov siab oxidative, uas ua lub luag haujlwm tseem ceeb hauv lub hnub nyoog kev paub txog kev poob qis hauv cov kab mob neuroinflammation-txog neurodegenerative xws li Alzheimer's thiab Parkinson's kab mob (Barnham li al., 2004). Cov enzymes tseem ceeb antioxidant, suav nrog superoxide dismutase (SOD) thiab catalase (CAT), raug suav tias yog thawj kab ntawm kev tiv thaiv antioxidant tiv thaiv ROS hauv vivo thaum oxidative puas tsuaj.

SOD tuaj yeem hloov superoxide anion rau hydrogen peroxide, uas tom qab ntawd tau khawb los ntawm CAT (Ighodaro thiab Akinloye, 2018). MDA yog lwm qhov kev paub zoo ntawm oxidative puas tsuaj nyob rau hauv cov xwm txheej ntawm oxidative kev nyuaj siab (Chung li al., 2010). TSIS ua lub luag haujlwm tseem ceeb hauv kev kawm los ntawm kev txhawb nqa lub zog mus sij hawm ntev hauv hippocampus (Bon thiab Garthwaite, 2003), nrog rau kev koom tes hauv intracellular signaling hauv neurons (Feil thiab Kleppisch, 2008). Interestingly, ib qho txawv txav nyob rau hauv reactive nitrogen hom txhaum cai apoptotic cell tuag los ntawm nitrosative raug mob rau neurons (Nakagawa thiab Yokozawa, 2002).

Kev soj ntsuam ntxiv tau qhia tias LPS cov thawj coj ua rau muaj kev cuam tshuam loj ntawm cov tshuaj tiv thaiv antioxidant catalase thiab overactivity ntawm qee cov enzymes xws li LPO thiab NO. Cov txiaj ntsig pom tau tuaj yeem yog vim qhov tshwm sim ntawm neuroinflammation-induced activation ntawm ROS hauv hippocampus. Raws li qhia hauv Fig.7 (a) thiab Fig.7 (b) DHQ-2 ug/kg thim rov qab LPS-enhanced CAT thiab LPO cov dej num. LPS-induced nce nyob rau hauv tsis muaj kev ua si raug txo los ntawm DHQ-1 thiab 2 ug/kg xwb Fig. 7 (c).

Cov txiaj ntsig tau pom tias DHQ muaj cov cuab yeej antioxidant raws li tau tshaj tawm ua ntej (Weidmann, 2012). LPS yog ib tug muaj zog activator ntawm microglia thiab up-regulates elaborations ntawm pro-inflammatory cytokines, xws li IL-6 thiab qog necrosis factor- (TNF- ) (Monje li al., 2003). Peb cov kev tshawb fawb tau pom tias kev tswj hwm LPS ua rau muaj kev nce ntxiv hauv qib IL-6 hauv hippocampus. Raws li pom hauv daim duab 6 DHQ-2 ug/kg txo qis IL{10}} qib hauv hippocampus. Cov txiaj ntsig tau pom tias DHQ muaj cov tshuaj tiv thaiv neuroinflammatory (Sah li al., 2011).

Cov nyhuv no ntawm DHQ tuaj yeem raug ntaus nqi vim tias nws cov kev ua haujlwm los tiv thaiv oxidant raws li ROS scavenging ua rau txo qis hauv IL-6 (Chen et al., 2014; Jain et al., 2009). Nyob rau yav tom ntej, cov txiaj ntsig ntawm DHQ ntawm LPS thiab amyloid beta-induced activation ntawm NF-kappa B ntawm tus xov tooj hu-zoo li receptor-4 ua kom nyob rau hauv lub microglial hlwb tuaj yeem tshawb xyuas raws li NF-kappa B yog ib qho ntawm cov peev xwm. Lub hom phiaj rau neuroinflammation thiab lwm yam teeb meem xws li dementia (Kim li al., 2015).

5. Cov lus xaus

DHQ tau txhim kho LPS-induced memory impairment thiab kev ntxhov siab zoo li tus cwj pwm hauv nas. Nws tau txo qis LPS-induced cholinergic dysfunction hauv hippocampus. Nws kuj tau pom tias muaj cov haujlwm antioxidant. DHQ tau qhia txog kev tiv thaiv neuroinflammatory kev ua los ntawm kev txo IL-6 ib qho tseem ceeb cytokine koom nrog hauv neuroinflamation. Li no, cov pov thawj preclinical taw qhia rau DHQ ua tus neeg sib tw muaj peev xwm hauv kev tswj hwm ntawm neuroinflammation thiab lwm yam kab mob neurodegenerative uas cuam tshuam nrog kev nco tsis zoo.

Lub mechanism ntawm Cistanche neuroprotection nyhuv

Cistanche yog ib hom tshuaj suav tshuaj suav tshuaj uas tau pom tias muaj cov teebmeem neuroprotective. Qhov tseeb mechanism ntawm nws qhov kev txiav txim tsis tau nkag siab tag nrho, tab sis muaj cov pov thawj loj hlob tuaj tias nws yuav muaj feem cuam tshuam nrog nws lub peev xwm los ua kom cov lus qhia ntawm cov teeb meem neurotrophic thiab tswj qee yam kev taw qhia hauv lub hlwb.

Ib qho ntawm cov tseem ceeb neurotrophic yam uas Cistanche tau pom tias nce ntxiv yog lub hlwb-derived neurotrophic factor (BDNF). BDNF yog cov protein uas ua lub luag haujlwm tseem ceeb hauv kev loj hlob, kev sib txawv, thiab kev saib xyuas cov neurons hauv lub hlwb. Cov kev tshawb fawb tau pom tias thaum qib BDNF siab dua, muaj ntau dua neuronal ciaj sia taus thiab plasticity, uas tuaj yeem pab tiv thaiv neurodegeneration.

Cistanche kuj tseem tuaj yeem tswj hwm qee yam kev taw qhia hauv lub hlwb uas koom nrog hauv cell survival thiab apoptosis (programmed cell tuag). Piv txwv li, nws tau pom tias inhibit qhov kev ua ntawm c-Jun N-terminal kinase (JNK) txoj kev, uas tuaj yeem ua rau tuag ntawm neurons nyob rau hauv qee yam mob. Los ntawm inhibiting JNK, Cistanche tuaj yeem pab tiv thaiv cov neurons los ntawm kev puas tsuaj thiab tswj lawv txoj sia.

Tsis tas li ntawd, Cistanche tau pom tias muaj cov tshuaj tiv thaiv kab mob thiab tshuaj tua kab mob antioxidant, uas tuaj yeem pab ntxiv los tiv thaiv cov neurons tiv thaiv kev puas tsuaj thiab tswj lawv txoj haujlwm. Cov khoom no ua rau Cistanche ua tus neeg sawv cev kho mob zoo rau kev kho mob ntawm cov kab mob neurodegenerative xws li Alzheimer's thiab Parkinson's disease.

Qadir Alam, Sairam Krishnamurthy *

Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, UP, India