Cov nyhuv ntawm Cistanche Tubulosa Extracts Rau Txiv neej Kev Ua Haujlwm Kev Ua Haujlwm hauv Streptozotocin-Nicotinamide-Induced Diabetic Rats-Ⅱ

Sep 04, 2024

3.2. Hauv Vivo Analysis

3.2.1. Cov teebmeem ntawm CTE ntawm lub cev hnyav thiab calorie kom tsawg

Tom qab 6 lub lis piam ntawm kev sim, pawg neeg mob ntshav qab zib (HFD-DM) tau pom lub cev hnyav dua li pawg tswj hwm. Pawg HFD-DME4 tau pom lub cev hnyav dua li HFD-DM thiab HFD-DMER pawg (Daim duab 7a). Cov calorie kom tsawg ntawm pawg tswj tau qis dua li lwm pab pawg. Tsis muaj qhov sib txawv tseem ceeb ntawm kev noj calorie ntawm lwm tsib pawg (Daim duab 7b).

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3.2.2. Qhov ncauj Glucose Tolerance Test (OGTT) txhawm rau txiav txim siab qhov ua tau zoo ntawm cov ntshav qab zib

Qhov kev kuaj ntshav qabzib hauv qhov ncauj (OGTT) yog siv los ua cov cuab yeej cog lus rau kev kuaj ntshav qab zib mellitus. Kev nce qib ntawm cov piam thaj hauv cov ntshav qhia txog kev mob ntshav qab zib. Raws li pom nyob rau hauv daim duab 8a, cov ntshav plasma qabzib qis dua hauv pawg CTE dua li hauv pawg DM ntawm 0, 30, 90, thiab 120 min. Tsis tas li ntawd, thaj tsam hauv qab ntawm qhov nkhaus (AUC) ntawm cov ntshav qabzib concentration pom tau tias hauv pawg CTE thiab RSG, cov ntshav qabzib nce siab tau nce (Daim duab 8b).

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3.2.3. Tag nrho cov ntshav qabzib hauv ntshav, cov roj (cholesterol) thiab triglycerides

Cov ntshav qabzib yoo mov qib ntshav qabzib siab dua hauv pawg DM thiab qis dua hauv DME2 pawg (tsuas yog tswj hwm) dua li lwm tus. Tsis muaj qhov sib txawv tseem ceeb hauv tag nrho cov roj cholesterol ntawm cov pab pawg tshwj tsis yog rau pawg DME4. Hauv pawg DME4, qib roj cholesterol qis dua lwm tus. Cov theem ntawm triglycerides tau siab dua hauv pawg DM thiab qis dua hauv DME4 pawg thiab cov ntsiab lus triglyceride tau txo qis nrog kev nce hauv cov concentration ntawm CTE (Table 2). Cov txiaj ntsig tau pom tias qib ntawm plasma qabzib, roj cholesterol, thiab triglycerides siab dua hauv pawg DM thiab qib tau txo qis hauv kev kho nrog CTE.

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3.2.4. Plasma Insulin Levels, Plasma Leptin Level, Thiab Homeostasis Model Assessment–Insulin Resistance (HOMA-IR) Values

Cov qib ntawm plasma insulin, leptin, thiab HOMA-IR qhov tseem ceeb tau qhia hauv Table 3. Cov pab pawg DM muaj cov ntshav plasma insulin ntau dua thiab plasma leptin ntau dua li pawg tswj hwm. HOMA-IR Performance index kuj tseem ceeb dua hauv pawg DM. Cov ntshav plasma insulin, leptin, thiab HOMA-IR qhov tseem ceeb tau txo qis nrog kev nce hauv cov concentration ntawm CTE. Plasma leptin tau txo qis hauv pawg CTE tab sis cov pab pawg tshuaj RSG (DMR) tsis pom qhov txawv ntawm pawg DM.

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3.2.5. Cov nyhuv ntawm CTE Ntawm Plasma LH Thiab Testosterone Levels Hauv Cov Kab Mob Ntshav Qab Zib

Raws li qhia hauv Table 4, qhov concentrations ntawm testosterone hauv cov nas mob ntshav qab zib (DM) tau txo qis, thaumqhov concentrations ntawm testosterone tau nce ntauntawm ntau koob tshuaj CTE. Tsis tas li ntawd, cov txiaj ntsig tau pom qhov txo qis ntawm qib LH hauv DM pawg piv rau DMR, DME1, DME2, thiab DME4. LH ntau lawm ntau dua hauv DME4 pawg.

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3.2.6. Cov nyhuv ntawm CTE Ntawm Cov phev Parameters ntawm Diabetic nas

Cov txiaj ntsig kev sim tau pom tias pawg DM muaj qhov txo qis hauv phev pes tsawg thiab kev txav mus los ntau dua li pawg tswj hwm thaum cov phev txawv txav tau nce ntau hauv pawg DM. Interestingly, tus phev naj npawb, phev motility, thiab cov phev txawv txav tus nqi ntawm DMR pab pawg neeg txhim kho tab sis cov phev motility tsis mus txog ib tug tseem ceeb raws li piv rau DME4. DME2 tau pom cov phev suav zoo dua li txhua tus ntawm lawv thiab qhov kev txav mus los tau nce ntxiv hauv pawg DME4. Tsis muaj qhov sib txawv tseem ceeb ntawm tus lej ntawm cov phev txawv txav ntawm RSG- thiab CTE-kho pab pawg (Table 5).

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3.2.7 ib. Cov txiaj ntsig ntawm CTE Ntawm Lub Morphology Ntawm Seminiferous Tubules Hauv Cov Kab Mob Ntshav Qab Zib

Daim duab 9 qhia txog H&E staining ntawm seem testis. Cov xub dub qhia txog Leydig cell thiab cov xub dawb qhia txog Sertoli cell. Ob leeg Leydig cell thiab Sertoli cell nyob rau hauv pawg DM tau pom qhov tseem ceeb atrophy thiab kab noj hniav tau pom hauv lumen. Cov qauv ntawm Leydig hlwb thiab Sertoli tau rov qab los hauv CTE- thiab RSG-kho pab pawg. Lub thickness ntawm lub seminiferous tubule yog siab dua nyob rau hauv CTE thiab RSG pawg tshaj nyob rau hauv DM pawg.

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3.2.8 ib. Cov nyhuv ntawm CTE Ntawm KiSS1, GPR54, SOCS-3, Thiab SIRT1 MRNAs Hauv Hypothalamus Ntawm Cov Kab Mob Ntshav Qab Zib

Kev qhia ntawm KiSS1 (Daim duab 10a), GPR54 (Daim duab 10b), SOCS-3 (Daim duab 10d), thiab SIRT1 (Daim duab 10c) tau qhia hauv daim duab 10. Qhov kev qhia mRNA ntawm KiSS1 thiab receptor GPR54 hauv cov nas mob ntshav qab zib yog qis dua hauv pawg tswj hwm. KiSS1 thiab GPR 54 mRNA qhia theem hauv DMR, DME1, DME2, thiab DME4 tau nce ntau. Tshwj xeeb, GPR54 mRNA qhia tau nce ntau hauv DME4 thiab yuav luag zoo ib yam li pawg tswj hwm.

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Qhov kev sim no tau tshawb fawb ntxiv txog qhov nyiaj ntawm SOCS-3 thiab SIRT1 mRNAs hauv hypothalamus ntawm nas. Kev qhia ntawm SOCS-3 mRNA hauv cov nas mob ntshav qab zib tau nce ntxiv qhia tias leptin impedance hnyav dua. Cov pab pawg DMR, DME1, DME2, thiab DME4 tau pom tias muaj kev txhim kho tseem ceeb thaum piv rau pab pawg neeg mob ntshav qab zib. Qhov kev qhia SIRT1 mRNA hauv pawg DM tau txo qis thiab tau nce ntxiv hauv DME1 thiab DME4 pawg.

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3.2.9 ib. Cov nyhuv ntawm CTE Ntawm Antioxidant Enzymes Hauv Plasma Thiab Testis Ntawm Cov Kab Mob Ntshav Qab Zib

Table 6 qhia tau hais tias cov plasma SOD kev ua, kev ua GPx, thiab catalase kev ua ntawm cov nas ntshav qab zib tau txo qis thiab cov dej num tau nce hauv CTE- thiab RSG-kho pab pawg. Ntxiv rau qhov no, DME4 tau pom muaj kev txhim kho tseem ceeb hauv GPx kev ua si dua li lwm tus. Cov txiaj ntsig tau pom tias SOD thiab catalase cov dej num hauv cov nas mob ntshav qab zib tau poob qis tom qab rau lub lis piam. SOD thiab catalase kev ua ntawm pawg DMR tsis mus txog qib tseem ceeb. Cov pab pawg kho CTE tau pom tias muaj kev txhim kho tseem ceeb hauv SOD thiab catalase kev ua haujlwm. Kev ua ub no ntawm catalase thiab SOD hauv CTE pawg kuj tau pom hauv testis (Table 7). Kev ua haujlwm siab tshaj plaws ntawm SOD thiab catalase tau pom hauv pawg DME1 thiab DME2 pawg raws li.

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3.2.10. Cov teebmeem ntawm CTE Ntawm Oxidative Stress thiab Inflammation Hauv Plasma Thiab Testis Ntawm Cov Kab Mob Ntshav Qab Zib

Nitric oxide (NO) ntau lawm hauv plasma (Daim duab 11a) thiab testis (Daim duab 11b) tau pom nyob rau hauv daim duab 11. Kev tsim tawm ntawm NO hauv pawg DM tau nce ntau hauv cov ntshav testis thiab ntshav piv rau pawg tswj hwm. Kev txo qis ntawm NO ntau lawm tau pom nyob rau hauv DME1, DME2, thiab DME4 pawg (hauv plasma). Pab pawg DMR kuj tau pom qhov txo qis hauv NO ntau lawm. Nyob rau hauv cov ntaub ntawv ntawm lub testis, muaj ib tug me ntsis txo ntawm NO ntau lawm tau pom nyob rau hauv CTE pawg, whereas pawg DMR tsis ho txo ​​NO ntau lawm.

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Raws li pom nyob rau hauv daim duab 12 thiab 13, theem ntawm TNF- thiab IL-6 tau nce ntau hauv cov nas mob ntshav qab zib (ob leeg hauv plasma thiab testis), qhia tias qhov mob hnyav dua. Hauv plasma, qib TNF- zoo ib yam hauv CTE- thiab RSG-kho pab pawg (Daim duab 12a). Cov pab pawg CTE tseem ceeb (tshwj xeeb tshaj yog DME2) txo qis theem ntawm TNF- hauv qhov testis (Daim duab 12b). Qib ntawm IL-6 tau txo qis hauv cov ntshav ntawm CTE thiab RSG pawg (Daim duab 13a). Nyob rau hauv lub testis, muaj ib tug qauv mus rau ib tug txo nyob rau hauv lub theem ntawm IL-6, tab sis qhov no tsis mus txog ib tug tseem ceeb theem (Daim duab 13b).

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3.2.1.1. Cov teebmeem ntawm CTE Ntawm Oxidative Stress thiab Inflammation Nyob rau hauv Spermatozoa Ntawm Cov Kab Mob Ntshav Qab Zib Induced Los Ntawm Kev Noj Qab Haus Huv Zoo

Daim duab 14 qhia txog cov ntsiab lus superoxide anion hauv nas phev. Cov txiaj ntsig tau pom tias superoxide anion ntau lawm hauv cov phev ntawm cov nas ntshav qab zib tau nce ntxiv thiab tsis muaj kev txhim kho tseem ceeb hauv pawg DMR. DME1 thiab DME4 pawg pom tau txo qis kev tsim tawm ntawm superoxide anion.

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3.2.12. Cov teebmeem ntawm CTE Ntawm Lipid Peroxidation Hauv Spermatozoa Ntawm Cov Kab Mob Ntshav Qab Zib Induced Los Ntawm Kev Noj Qab Haus Huv

Cov kev tshawb fawb tau pom tias lipid peroxidation tau nce ntxiv hauv cov neeg mob ntshav qab zib hom 1 thiab hom 2 [19]. Qib malondialdehyde (MDA) hauv ntshav, phev, thiab testis yog qhia nyob rau hauv Table 8. MDA theem nyob rau hauv plasma, testis, thiab phev ntawm pawg DM tau nce siab dua thiab kev kho mob nrog CTE thiab RSG txo qhov tsim ntawm MDA. Kev txo qis tseem ceeb tau pom hauv DME4 thiab DMEI pawg hauv plasma. Txoj kev tshawb no pom tias cov nas mob ntshav qab zib tsis tsuas yog nce qib ntawm lipid peroxidation hauv plasma tab sis kuj nce hauv cov qog thiab phev. Kev txhim kho tseem ceeb tau pom ntawm ntau qhov koob tshuaj CTE.

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4. Kev sib tham

Mob ntshav qab zib yog ib yam kab mob ntev uas cuam tshuam nrog cov piam thaj hauv cov ntshav siab. Qhov tsis sib xws ntawm cov tshuaj tiv thaiv antioxidant thiab ROS yuav ua rau cov mob hu ua oxidative stress. Superoxide, hydroxyl radical, hydrogen peroxide, nitric oxide, thiab singlet oxygen yog qee qhov piv txwv ntawm ROS uas yuav ua rau muaj mob ntshav qab zib los ntawm oxidative stress [20].Cistanche tubulosayog cov nroj tsuag suab puam uas muaj cov khoom siv xws lipolysaccharides, oligosaccharides, phenylethanoid glycosides (echinacoside, verbascoside), palmitic acid, linoleic acid, iridoids, alditols, thiab lignans. Cov nroj tsuag no muaj peev xwm tsim tau cov tshuaj tiv thaiv kab mob, neuroprotective, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tiv thaiv qog, thiab cov teebmeem immunomodulatory [21]. Cov ntaub ntawv tshawb fawb qhia tias phenylethanoid glycosides los ntawm Cistanche tubulosa yog qhov laj thawj tseem ceeb rau kev ua haujlwm antioxidant [22]. Resveratrol (RES) thiab rosiglitazone (RSG) tau raug coj los ua kev tswj xyuas zoo rau hauv vitro thiab hauv vivo kev tshawb fawb feem. RSG yog cov tshuaj insulin muaj zog thiab muaj kev sib raug zoo ntawm isoform ntawm peroxisome proliferator-activated receptor (PPARc). Nws tswj hyperglycemia hauv cov neeg mob ntshav qab zib [23]. RES muaj tej yam ntuj tso antioxidant thiab ua raws li vasodilator, tswj lipoprotein metabolism, inhibiting platelet aggregation, thiab tiv thaiv qog noj ntshav [24,25]. Peb qhov kev tshawb fawb tau qhia tias ECH qhia tau hais tias muaj kev cuam tshuam zoo tshaj plaws ntawm cov khoom siv hluav taws xob ntau dua li CTE thiab RES (Daim duab 1). Nws kuj tseem nkag siab tias ECH tsis ua rau muaj kev cuam tshuam loj rau LC-540 thiab TM3 Leydig hlwb (Daim duab 2).

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AGEs tau siv los ua kom muaj kev ntxhov siab hauv Leydig hlwb. Kev tsim cov AGEs, o, oxidative kev nyuaj siab, thiab ntshav qab zib yog sib cuam tshuam. Cov mob hyperglycemic ntawm ntshav qab zib txhawb kev raug mob ntawm tes los ntawm kev tsim cov AGEs thiab oxidative kev nyuaj siab. AGEs induce cell toxicity, uas ntxiv txhawb kev tiv thaiv kab mob ntawm tes thiab cell tuag. Ib qib siab ntawm AGEs txhawb kev qhia ntawm ob hom receptors hu ua RAGE thiab AGER1 [26]. Lub dripping thiab tom qab hloov ntawm ib qho hluav taws xob los ntawm mitochondrial respiratory saw mus rau molecular oxygen thaum lub sij hawm oxidative kev nyuaj siab tshwm sim nyob rau hauv lub tsim ntawm ib tug superoxide anion. Peb cov txiaj ntsig tau pom tias kev tsim cov superoxide anion tshwm sim los ntawm AGEs tau nce hauv pawg tswj hwm thiab kev txhim kho ntxiv tau pom nrog kev kho ECH thiab RES. Raws li peb txoj kev tshawb fawb, nws tau nkag siab tias superoxide (Daim duab 3) thiab H2O2 (Daim duab 4) tsim los ntawm AGEs tau txo qis hauv qhov muaj ECH thiab RES.

NF-κB yog lub npe hu ua tus neeg nruab nrab tseem ceeb ntawm kev mob o cuam tshuam nrog ntshav qab zib [27]. Kev qhia ntawm NF-κB ua rau kev ua haujlwm tsis zoo ntawm tes thiab kev tuag ntawm tes. Kev ua kom NF-κB los ntawm oxidative kev nyuaj siab txhawb cov lus teb pro-inflammatory, upregulation ntawm endothelin, thiab apoptosis [28]. Kev qhia ntawm RAGE thiab NF-κB tau nce hauv AGE-stimulated pab pawg thiab kev txo qis tom qab tau pom hauv ECH- thiab RES-kho hlwb (Daim duab 5).

Testosteroneyog ib qho anabolic steroid thiab thawjtxiv neej pw ua ke hormonesynthesized los ntawm cov cholesterol. Cov txheej txheem pib nrog cov oxidative cleavage ntawm cov cholesterol sab saw los ntawm cov cholesterol sab saw cleavage noob (CYP11A). Cov noob no nyob hauv thaj chaw mitochondrial thiab hloov cov roj cholesterol mus rau hauv pregnenolone. Tom ntej no, CYP17A1 noob los ntawm endoplasmic reticulum tshem tawm ob qho ntxiv carbon atoms thiab tsim ntau yam C19 steroids. Ntxiv rau qhov no, pregnenolone yog oxidized los tsim androstenedione/progesterone los ntawm hydroxysteroid dehydrogenase (3- -HSD). Thaum kawg, testosterone yog tsim los ntawm kev txo qis ntawm pawg keto hauv 17th carbon txoj hauj lwm ntawm androstenedione los ntawm 17-beta-hydroxysteroid dehydrogenase (17- -HSD). Leydig hlwb koom nrog hauv kev tsim khoom loj ntawm testosterone. Kev hloov cov roj (cholesterol) mus rau hauv lub mitochondrial membrane sab hauv yuav tsum tau ua ntawm steroidogenic acute regulatory protein (StAR). Cov kev tshawb fawb tam sim no qhia tau hais tias kev qhia ntawm StAR, CYP11A1, CYP17A1, thiab HSD17 3 tau txo qis hauv AGE-kho hlwb (tswj) thiab muaj qhov nce loj heev tau pom hauv ECH- thiab RES-kho hlwb (Daim duab 6) . Yog li, cov txiaj ntsig tau pom tias cov khoom tsim tawmTestosterone tau nce hauv ECH- thiab RES-kho pab pawg. 

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Thaum mob ntshav qab zib mellitus, kev thauj cov piam thaj mus rau hauv nruab nrog cev raug txwv thiab vim li ntawd, cov piam thaj nce ntxiv [29]. Yog li, hyperglycemic mob yog ib qho ntawm cov cim tseem ceeb rau kev kuaj ntshav qab zib. Peb cov kev tshawb fawb qhia tau hais tias cov ntshav qabzib hauv cov ntshav tau nce ntxiv hauv pawg neeg mob ntshav qab zib thiab AUC ntawm pawg DM tau nce siab dua li lwm pab pawg (Daim duab 8). Nrog rau plasma qabzib, tag nrho cov roj cholesterol thiab triglyceride cov ntsiab lus tau nce ntxiv hauv pawg DM (Table 2). Atherosclerosis yog yooj yim los ntawm kev nce qib ntawm cov cholesterol thiab triglycerides [30]. Txawm li cas los xij, qib roj cholesterol thiab triglycerides tau txo qis hauv CTE- thiab RSG-kho pab pawg. Cov ntsiab lus triglyceride ntawm DME4 pawg tau mus txog yuav luag cov txiaj ntsig zoo sib xws rau pawg tswj hwm.

Insulin yog ib yam tshuaj uas tsim los ntawm cov hlwb ntawm lub txiav thiab ua haujlwm los tswj cov ntshav qab zib hauv lub cev thaum leptin yog ib yam tshuaj uas tsim los ntawm cov adipocytes uas muaj peev xwm tswj hwm kev noj zaub mov thiab siv zog. Cov kev tshawb fawb qhia tias leptin koom nrog hauv pathophysiology ntawm kev rog rog thiab muaj kev cuam tshuam zoo ntawm leptin thiab insulin [31]. Peb cov kev tshawb fawb qhia tau hais tias qib ntawm plasma inulin thiab leptin yog siab dua hauv pawg DM thiab qib insulin tau txo qis nrog kev nce hauv cov concentration ntawm CTE. Pawg RSG tsis qhia qhov txawv ntawm pawg DM. Cov tshuaj insulin tsis kam thiab kev ua haujlwm ntawm tes raug soj ntsuam los ntawm HOMA-IR txoj kev. Tus nqi HOMA-IR tau nce hauv pawg DM thiab txawv ntawm lwm pawg (Table 3).

DM cuam tshuam rau kev ua me nyuam los ntawm kev hloov pauv hormonal hauv HPG axis thiab cov kev tshawb fawb tau qhia tias cov tshuaj insulin hauv cov qe ntshav tseem cuam tshuam los ntawm ntshav qab zib. Nws yog tus cwj pwm los ntawm Sertoli cell vacuolization, nce DNA fragmentation, impaired spermatogenesis, thiab nce kab mob cell depletion. Kev ntxhov siab oxidative kuj tseem ua rau muaj qhov txawv txav hauv kev ua menyuam yaus [32]. Cov txheej txheem ntawm kev tsim cov phev nyob rau hauv cov txiv neej reproductive organ (testes) yog hu ua spermatogenesis. Lub testis yog tsim los ntawm nruj coiled tubules hu ua seminiferous tubules. Sertoli hlwb pom nyob rau hauv cov phab ntsa ntawm lub seminiferous tubule thiab muab khoom noj rau cov phev tsis paub qab hau. Kev tshawb xyuas ntawm cov phev tsis tau qhia tias cov phev thiab kev txav mus los tsawg zuj zus thiab qhov txawv txav tau nce hauv pawg DM (Table 5). Ib qho kev cuam tshuam sib txawv tau pom hauv CTE- thiab RSG-kho pab pawg. Ob leeg Leydig cell thiab Sertoli hlwb hauv DM pab pawg tau pom qhov tseem ceeb atrophy thiab cov kab noj hniav tau pom hauv lumen. Lub thickness ntawm seminiferous tubule kuj txo qis hauv pawg DM. Ib qho kev txhim kho tau pom nyob hauv CTE- thiab RSG-kho pab pawg (Daim duab 9). Ntxiv rau qhov no, qib ntawm LH thiab testosterone txo qis hauv pawg DM thiab qib nce hauv CTE-kho pab pawg (Table 4). Hauv cov txiv neej, qis qis testosterone thiab qis LH mem tes zaus feem ntau cuam tshuam nrog kev rog thiab ntshav qab zib mellitus hom 2 [33].

Kisspeptins encoded los ntawm KiSS1 noob yog lub npe hu ua lub zog stimulator ntawm HPG axis thiab ib qho kev hloov hauv cov noob kisspeptin yuav ua rau qis qis ntawm kev sib deev steroids thiab gonadotropin. Cov kev tshawb fawb pom tau tias hauv STZ-vim cov nas mob ntshav qab zib, Kiss1 mRNA qib tau txo qis [33]. Kev pib thiab kev saib xyuas ntawm mammalian infertility yog txuas nrog G-protein coupled receptor 54 (GPR54). Kev hloov pauv hauv GPR 54 yog tus cwj pwm los ntawm qhov tsis muaj kev sib deev loj hlob thiab qib qis ntawm cov tshuaj gonadotropic (LH thiab FSH). Pro-inflammatory cytokines xws li IL-6 thiab TNF- nce-tswj cov lus qhia ntawm kev tawm tsam ntawm cytokine signaling 3 (SOCS3) cuam tshuam rau hauv qhov mob-kho cov tshuaj insulin tsis kam hauv daim siab thiab adipocytes [34]. SIRT 1 yog cov noob caj noob ces cuam tshuam nrog kev tswj hwm ntawm ntau yam kab mob laus. Cov noob no tau nthuav tawm hauv cov hlwb ntawm cov txiav thiab tswj cov tshuaj insulin secretion thiab tiv thaiv apoptosis. Cov kev tshawb fawb tam sim no tau qhia tias qhov kev qhia ntawm KiSS1, GPR54, thiab SIRT1 tau txo qis hauv pawg DM, tab sis cov lus qhia tau nce hauv cov pab pawg kho CTE (Daim duab 10). Kev nce hauv SOCS-3 kab lus hauv pawg DM qhia tias muaj mob. Thawj qhov sib txuas molecular pom ntawm kev rog thiab mob yog TNF- . Li no, nce qib ntawm TNF- yog qhov qhia txog kev mob. Qhov txo qis ntawm cov cytokines pro-inflammatory xws li TNF- thiab IL-6 tau pom hauv CTE-kho pab pawg (Figures 12 thiab 13).

Qhov tsis sib xws ntawm ROS thiab antioxidants ua rau muaj mob ntshav qab zib. Superoxide dismutase (SOD), catalase (CAT), thiab glutathione peroxidase (GPX) yog lub npe hu ua thawj antioxidants lub luag hauj lwm rau kev tswj qhov zoo ROS qib [35]. Los ntawm cov txiaj ntsig, nws tau pom tias kev ua haujlwm ntawm cov tshuaj antioxidants tau qis dua hauv pawg DM. CT-kho pab pawg tau pom tias muaj kev txhim kho hauv kev tsim cov tshuaj antioxidants. Cov pab pawg kho mob RSG tsis pom muaj kev txhim kho tseem ceeb hauv kev ua haujlwm antioxidant (Table 6 thiab 7).

Nitric oxide (NO) paub tias yog ib qho tseem ceeb ROS uas ua rau muaj mob. Peb cov kev tshawb fawb taw qhia tias qib NO tau txo qis hauv cov pab pawg kho CTE (Daim duab 11). Cov txiaj ntsig tau pom tias cov ntsiab lus superoxide anion hauv cov phev ntawm cov nas ntshav qab zib tau nce ntxiv thiab tsis muaj kev txhim kho tseem ceeb tom qab kev tswj hwm ntawm RSG. Kev tsim cov superoxide tau txo qis hauv CTE pawg.

Kev txiav txim siab ntawm MDA yog qhov tseem ceeb heev rau kev ntsuas lipid peroxidation. Lipid peroxidation yog cov txheej txheem ntawm oxidation hauv lipids thiab thaum kawg ua rau cov cell puas. MDA yog tsim los ntawm lipid peroxidation ntawm polyunsaturated fatty acids. Cov kev tshawb fawb qhia tias qib MDA muaj feem cuam tshuam nrog lub hnub nyoog thiab qib ntshav qabzib ceev [36]. Txoj kev tshawb fawb tam sim no tau qhia tias CTE txhim kho lipid peroxidation hauv plasma, testis, thiab phev (Table 8).

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5. Cov lus xaus

Cov kev ntxhov siab oxidative thaum mob ntshav qab zib cuam tshuam rau txiv neej txoj kev loj hlob los ntawm phev tsis zoo thiab gonadal tsis ua haujlwm. Cistanche tubulosa yog cov nroj tsuag suab puam dav lees paub hauv Suav tshuaj vim nws cov tshuaj pharmacological.Echinacoside (ECH)yog lub ntsiab lus tseem ceeb ntawm CTE lub luag haujlwm rau nws cov tshuaj tiv thaiv antioxidant thiab tiv thaiv kab mob. Peb cov txiaj ntsig hauv vitro tau qhia tias ECH tau rov qab ua txoj hauv kev ntawm testosterone synthesis thiab txo qis qib ntawm NF-κB thiab RAGE protein qhia. ECH zoo inhibited zus tau tej cov superoxide anion thiab H2O2 nyob rau hauv Leydig hlwb. Cov kev tshawb fawb hauv vivo tau qhia tias ECH txo cov roj cholesterol, triglycerides, TNF- , thiab IL-6. Ntxiv rau qhov no, mRNA cov lus qhia hauv hypothalamus ntawm cov nas ntshav qab zib tau txhim kho tau zoo. Nws tseem ceeb heev uas ECH txo lipid peroxidation thiab txhim kho cov tshuaj insulin hauv cov txiv neej nas ntshav qab zib. Kev ua haujlwm antioxidant tau nce ntxiv hauv plasma thiab testis. Yog li ntawd, peb cov kev tshawb fawb tau pom tias ECH tau muab kev tiv thaiv zoo tiv thaiv kev ua me nyuam tsis zoo nyob rau hauv STZ-induced diabetes txiv neej nas.



Koj Tseem Yuav Zoo Li