Ultrasonic-assisted nanoencapsulation of kiwi leaves proanthocyanidins in liposome delivery system for enhanced biostability and bioavailability.

The poor biostability and bioavailability of proanthocyanidins limit their application. In this study, it was hypothesized that encapsulation in lecithin-based nanoliposomes using ultrasonic technology improves the above properties. Based on preliminary experiments, the effects of lecithin mass ratio (1-9%, wt.), pH (3.2-6.8), ultrasonic power (0-540 W), and time (0-10 min) on biostability and bioavailability of purified kiwi leaves proanthocyanidins (PKLPs) were determined. Nanoliposomes prepared optimally with lecithin (5%, wt.), pH = 3.2, ultrasonic power (270 W), and time (5 min) demonstrated a significantly (p < 0.05) improved physicochemical stability, homogeneity, and high encapsulation efficiency (73.84%) relative to control. The PKLPs bioaccessibility during in vitro digestion increased by 2.28-3.07-fold, with a remarkable sustained release and delivery to the small intestine. Similar results were obtained by in vivo analyses, showing over 200% increase in PKLPs bioaccessibility compared to the control. Thus, PKLPs-loaded nanoliposomes are promising candidates for foods and supplements for novel applications.

Case Report: Torsade de Pointes Induced by the Third-Generation Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Osimertinib Combined With Litsea Cubeba.

Torsades de Pointes (TdP) occurred in a 68-year-old female with epidermal growth factor receptor (EGFR) mutant lung cancer administered osimertinib, the third-generation EGFR tyrosine kinase inhibitor (TKI). Electrocardiogram (ECG) recorded at Tdp showed QT prolongation (QTc = 515 ms), to which a Traditional Chinese Medicine (TCM) named "Litsea Cubeba" may have contributed. After discontinuation of osimertinib and Litsea Cubeba, magnesium supplementation, potassium supplementation, lidocaine infusion, and the pacemaker frequency adjustment, Tdp terminated. However, QT prolongation sustained at discharge (QTc = 528 ms), partly because of the emergency use of amiodarone. Osimertinib may prolong the QT interval leading to TdP, especially when multiple risk factors to lengthen QT interval are incidentally overlapped. Thus, regular monitoring of ECG and appropriate management of concomitant drugs are highly recommended.

Catalytic asymmetric coupling of vinylogous species via deconjugated butenolide addition to vinylogous imines in situ generated from arylsulfonyl indoles.

An efficient catalytic asymmetric coupling of vinylogous species is developed via deconjugated butenolide addition to vinylogous imines in situ generated from arylsulfonyl indoles. With quinine-derived bifunctional squaramide as the catalyst, a series of structurally diverse enantioenriched sec-alkyl-3-substituted indoles containing valuable γ,γ-disubstituted butenolide moieties and adjacent quaternary-tertiary stereocenters are obtained in synthetically viable results (up to 97% yield, 77 : 23 dr and 97% ee).

Benzylidene succinimides as 3C synthons for the asymmetric tandem Mannich reaction/transamidation of cyclic trifluoromethyl ketimines to obtain F3C-containing polycyclic dihydroquinazolinones.

By taking advantage of benzylidene succinimides as a new class of 3C synthons, a highly diastereo- and enantioselective tandem Mannich reaction/transamidation has been established by reacting them with cyclic trifluoromethyl N-acyl ketimines. Using a Cinchona alkaloid-derived squaramide as the catalyst, the tandem reaction proceeded smoothly under mild conditions and afforded a range of F3C-containing chiral polycyclic dihydroquinazolinones with excellent results (up to 99% yield, all cases >20 : 1 dr, up to 99% ee).

Organocatalytic asymmetric tandem α-functionalization/1,3-proton shift reaction of benzylidene succinimides with ß-trifluoromethyl enones.

A bifunctional thiourea-catalyzed asymmetric tandem α-functionalization/1,3-proton shift reaction of benzylidene succinimides with ß-trifluoromethyl enones has been developed. A series of F3C-containing chiral Rauhut-Currier type products were obtained in moderate to high yields (up to 98%) with excellent enantioselectivities (up to >99% ee). This represents the first example of benzylidene succinimides undergoing tandem α-functionalization/1,3-proton shift in catalytic enantioselective transformation.

Highly enantioselective sequential vinylogous aldol reaction/transesterification of methyl-substituted olefinic butyrolactones with isatins for the construction of chiral spirocyclic oxindole-dihydropyranones.

A highly stereoselective sequential vinylogous aldol reaction/transesterification of methyl-substituted olefinic butyrolactones and isatins was developed. With this developed protocol, a series of chiral spirocyclic oxindole-dihydropyranones were obtained in good to excellent yields (73-99%) and enantioselectivities (71-97% ee).

Characteristics of the HIV/AIDS Epidemic in Women Aged 15-49 Years from 2005 to 2012 in China.

OBJECTIVE: To describe the characteristics of the HIV/AIDS epidemic in women aged 15-49 years in China. METHODS: HIV/AIDS cases from 2005 to 2012 that fulfilled the inclusion and exclusion criteria were identified on the Chinese HIV/AIDS case reporting system. Descriptive and spatial analyses were performed. RESULTS: A total of 103,559 female HIV/AIDS cases were included in our study. Based on the descriptive analysis, between 2005 and 2012, the proportion of heterosexually acquired HIV infection among women (15-49 years) increased rapidly from 35.8% to 87.4%. Approximately 60% of these cases were infected through non-marital heterosexual contact. Among older women (40-49 years), a slightly increasing trend was identified. The spatial analysis detected 'hot spots' in the Xinjiang, Yunnan, Sichuan, Guangxi, and Chongqing provinces. The epidemic trends in these areas were predominately driven by heterosexual transmission. CONCLUSION: Non-marital heterosexual contact is a very important factor in the HIV/AIDS epidemic in women aged 15-49 years, and the HIV infection rate in older women is increasing. Several epidemic hot spots were detected in northwestern and southwestern China. Efficient interventions are needed to control the spread of HIV/AIDS among women living in these areas.

[Antioxidative effects of cysteinyl leukotriene receptor antagonists montelukast and HAMI 3379 on ischemic injury in rat cortical neurons in vitro].

OBJECTIVE: To investigate the antioxidative effects of two cysteinyl leukotriene receptors antagonists (CysLT1R and CysLT2R) montelukast and HAMI 3379 on ischemic injury of rat cortical neurons in vitro. METHODS: Cultured rat cortical neurons were pretreated with CysLT1R antagonist montelukast and CysLT2R antagonist HAMI 3379, and then exposed to oxygen-glucose deprivation/recovery (OGD/R）or H2O2. Reactive oxygen species (ROS) mitochondrial membrane potential (MMP) depolarization, neuronal viability and lactate dehydrogenase (LDH) release were determined. Meanwhile, RNA interference was used to inhibit the expression of CysLT1R and CysLT2R，and the effects were observed. RESULTS: ROS production in neurons was significantly increased after 1 h OGD, which reached the peak at 30 min and lasted for 1.5 h after recovery. Montelukast and HAMI 3379 at 0.01-1µmol/L moderately decreased OGD/R-induced ROS production (P<0.05). Montelukast mildly attenuated OGD/R-induced MMP depolarization (P<0.05)，but HAMI 3379 had no effect. H2O2 reduced neuronal viability and increased LDH release, namely inducing neuronal injury. Montelukast and HAMI 3379 at 0.1-1µmol/L moderately attenuated H2O2-induced neuronal injury (P<0.05). However, both CysLT1R siRNA and CysLT2R shRNA did not significantly affect the responses mentioned above. CONCLUSION: In ischemic neuronal injury, montelukast and HAMI 3379 exert a moderate antioxidative effect, and this effect may be receptor-independent.

[Effect of histone deacetylase inhibitor NL101 on rat neurons].

OBJECTIVE: To investigate the protective effect of histone deacetylase inhibitor NL101 on L-homocysteine (HCA)-induced toxicity in rat neurons, and the toxic effect on normal rat neurons. METHODS: In the presence of NL101 at various concentrations, HCA (5 mmol/L)-induced changes in cell density, necrosis, and viability were determined in the mixed cultures of rat cortical cells and the primary cultures of rat neurons. The direct effect of NL101 on primary neurons was also observed in the absence of HCA. Histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) was used as the control. After the treatments, cell viability, the density, and morphology of neurons and glial cells, and cell necrosis were determined. RESULTS: In the mixed cultures of cortical cells, NL101 had no effect on HCA (5 mmol/L)-induced cell number reduction at 0.001-10µmol/L; however, it significantly attenuated necrosis at 1-10 µmol/L, and increased neuronal number at 1 µmol/L. NL101 had no effect on the mixed cortical cells in the absence of HCA. In the primary neurons, NL101 reduced neuronal viability and mildly increased necrosis at 1-10 µmol/L in the absence of HCA, while it significantly attenuated HCA-induced neuronal viability reduction at 0.01-10 µmol/L and reduced neuronal necrosis at 1-10 µmol/L. The effects of NL101 were apparently similar to those of SAHA. CONCLUSION: NL101 has protective effect on HCA-induced neuronal injury but it is neurotoxic at high concentrations, which is similar to the typical histone deacetylase inhibitor SAHA.

Cysteinyl leukotriene receptor 1 mediates LTD4-induced activation of mouse microglial cells in vitro.

AIM: To investigate the roles of cysteinyl leukotriene receptors CysLT1R and CysLT2R in leukotriene D4 (LTD4)-induced activation of microglial cells in vitro. METHODS: Mouse microglial cell line BV2 was transfected with pcDNA3.1(+)-hCysLT1R or pcDNA3.1(+)-hCysLT2R. The expression of relevant mRNAs and proteins in the cells was detected using RT-PCR and Western blotting, respectively. Phagocytosis was determined with flow cytometry analysis. The release of interleukin-1ß (IL-1ß) from the cells was measured using an ELISA assay. RESULTS: The expression of CysLT1R or CysLT2R was considerably increased in the transfected BV2 cells, and the receptors were mainly distributed in the plasma membrane and cytosol. Treatment of the cells expressing CysLT1R or CysLT2R with CysLT receptor agonist LTD4 (0.1-100 nmol/L) concentration-dependently enhanced the phagocytosis, and increased mRNA expression and release of IL-1ß. Moreover, the responses of hCysLT1R-BV2 cells to LTD4 were significantly larger than those of hCysLT2R-BV2 or WT-BV2 cells. Pretreatment of hCysLT1R-BV2 cells with the selective CysLT1R antagonist montelukast (1 µmol/L) significantly blocked LTD4-induced phagocytosis as well as the mRNA expression and release of IL-1ß, whereas the selective CysLT2R antagonist HAMI 3379 (1 µmol/L) had no such effects. CONCLUSION: CysLT1R mediates LTD4-induced activation of BV2 cells, suggesting that CysLT1R antagonists may exert anti-inflammatory activity in brain diseases.

HAMI 3379, a CysLT2 receptor antagonist, attenuates ischemia-like neuronal injury by inhibiting microglial activation.

The cysteinyl leukotrienes (CysLTs) are inflammatory mediators closely associated with neuronal injury after brain ischemia through the activation of their receptors, CysLT1R and CysLT2R. Here we investigated the involvement of both receptors in oxygen-glucose deprivation/recovery (OGD/R)-induced ischemic neuronal injury and the effect of the novel CysLT2R antagonist HAMI 3379 [3-({[(1S,3S)-3- carboxycyclohexyl]amino}carbonyl)-4-(3-{4-[4-(cyclo-hexyloxy)butoxy]phenyl}propoxy)benzoic acid] in comparison with the CysLT1R antagonist montelukast. In primary neurons, neither the nonselective agonist leukotriene D4 (LTD4) nor the CysLT2R agonist N-methyl-leukotriene C4 (NMLTC4) induced neuronal injury, and HAMI 3379 did not affect OGD/R-induced neuronal injury. However, in addition to OGD/R, LTD4 and NMLTC4 induced cell injury and neuronal loss in mixed cultures of cortical cells, and neuronal loss and necrosis in neuron-microglial cocultures. Moreover, they induced phagocytosis and cytokine release (interleukin-1ß and tumor necrosis factor-α) from primary microglia, and conditioned medium from the treated microglia induced neuronal necrosis. HAMI 3379 inhibited all of these responses, and its effects were the same as those of CysLT2R interference by CysLT2R short hairpin RNA, indicating CysLT2R dependence. In comparison, montelukast moderately inhibited OGD/R-induced primary neuronal injury and most OGD/R- and LTD4-induced (but not NMLTC4-induced) responses in mixed cultures, cocultures, and microglia. The effects of montelukast were both dependent and independent of CysLT1Rs because interference by CysLT1R small interfering RNA had limited effects on neuronal injury in neuron-microglial cocultures and on cytokine release from microglia. Our findings indicated that HAMI 3379 effectively blocked CysLT2R-mediated microglial activation, thereby indirectly attenuating ischemic neuronal injury. Therefore, CysLT2R antagonists may represent a new type of therapeutic agent in the treatment of ischemic stroke.

Cerebral ischemia is exacerbated by extracellular nicotinamide phosphoribosyltransferase via a non-enzymatic mechanism.

Intracellular nicotinamide phosphoribosyltransferase (iNAMPT) in neuron has been known as a protective factor against cerebral ischemia through its enzymatic activity, but the role of central extracellular NAMPT (eNAMPT) is not clear. Here we show that eNAMPT protein level was elevated in the ischemic rat brain after middle-cerebral-artery occlusion (MCAO) and reperfusion, which can be traced to at least in part from blood circulation. Administration of recombinant NAMPT protein exacerbated MCAO-induced neuronal injury in rat brain, while exacerbated oxygen-glucose-deprivation (OGD) induced neuronal injury only in neuron-glial mixed culture, but not in neuron culture. In the mixed culture, NAMPT protein promoted TNF-α release in a time- and concentration-dependent fashion, while TNF-α neutralizing antibody protected OGD-induced, NAMPT-enhanced neuronal injury. Importantly, H247A mutant of NAMPT with essentially no enzymatic activity exerted similar effects on ischemic neuronal injury and TNF-α release as the wild type protein. Thus, eNAMPT is an injurious and inflammatory factor in cerebral ischemia and aggravates ischemic neuronal injury by triggering TNF-α release from glia cells, via a mechanism not related to NAMPT enzymatic activity.

Nicotinamide phosphoribosyltransferase may be involved in age-related brain diseases.

Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme for nicotinamide adenine dinucleotide (NAD) biosynthesis, and can be found either intracellularly (iNAMPT) or extracellularly (eNAMPT). Studies have shown that both iNAMPT and eNAMPT are implicated in aging and age-related diseases/disorders in the peripheral system. However, their functional roles in aged brain remain to be established. Here we showed that upon aging, NAMPT level increased in serum but decreased in brain, decreased in cortex and hippocampus but remained unchanged in cerebellum and striatum in brain, and increased in microglia but likely decreased in neuron. Accordingly, total NAD (tNAD) level significantly decreased in hippocampus, cerebellum and striatum in aged brain. Application of recombinant NAMPT, mimicking the elevated serum NAMPT level, enhanced the susceptibility of cerebral endothelial cells to ischemic injury, while inhibition of iNAMPT by FK866, a specific inhibitor, reduced intracellular NAD level and induced neuronal death. Taken together, we have revealed a region- and cell-specific change of NAMPT level in brain and serum upon aging, deduced its potential consequences, which suggests that NAMPT is a regulatory factor in aging and age-related brain diseases.

Intracerebroventricular injection of HAMI 3379, a selective cysteinyl leukotriene receptor 2 antagonist, protects against acute brain injury after focal cerebral ischemia in rats.

Cysteinyl leukotrienes (CysLTs) induce inflammatory responses by activating their receptors, CysLT(1)R and CysLT(2)R. We recently reported that CysLT(2)R is involved in neuronal injury, astrocytosis and microgliosis after focal cerebral ischemia in rats. Here, we determined whether HAMI 3379, a selective CysLT(2)R antagonist, protects against acute brain injury after focal cerebral ischemia in rats. We induced transient focal cerebral ischemia by 30 min of middle cerebral artery occlusion (MCAO), followed by 24h of reperfusion. HAMI 3379 (1, 10 or 100 ng) was injected intracerebroventricularly (i.c.v.) 30 min before MCAO, and the CysLT(1)R antagonist pranlukast (0.1mg/kg, i.p.) was used as a positive control. HAMI 3379 at 10 and 100 ng (but not at 1 ng) attenuated the neurological deficits, and reduced infarct volume, brain edema, IgG exudation, neuronal degeneration and neuronal loss. This protective effect was similar to that of pranlukast. Thus, HAMI 3339 at 10-100 ng i.c.v. is neuroprotective against acute brain injury after focal cerebral ischemia in rats. These findings suggest therapeutic potential for CysLT(2)R antagonists in the treatment of ischemic stroke.

Transforming growth factor ß1-induced astrocyte migration is mediated in part by activating 5-lipoxygenase and cysteinyl leukotriene receptor 1.

BACKGROUND: Transforming growth factor-ß 1 (TGF-ß 1) is an important regulator of cell migration and plays a role in the scarring response in injured brain. It is also reported that 5-lipoxygenase (5-LOX) and its products, cysteinyl leukotrienes (CysLTs, namely LTC4, LTD4 and LTE4), as well as cysteinyl leukotriene receptor 1 (CysLT1R) are closely associated with astrocyte proliferation and glial scar formation after brain injury. However, how these molecules act on astrocyte migration, an initial step of the scarring response, is unknown. To clarify this, we determined the roles of 5-LOX and CysLT1R in TGF-ß 1-induced astrocyte migration. METHODS: In primary cultures of rat astrocytes, the effects of TGF-ß 1 and CysLT receptor agonists on migration and proliferation were assayed, and the expression of 5-LOX, CysLT receptors and TGF-ß1 was detected. 5-LOX activation was analyzed by measuring its products (CysLTs) and applying its inhibitor. The role of CysLT1R was investigated by applying CysLT receptor antagonists and CysLT1R knockdown by small interfering RNA (siRNA). TGF-ß 1 release was assayed as well. RESULTS: TGF-ß 1-induced astrocyte migration was potentiated by LTD4, but attenuated by the 5-LOX inhibitor zileuton and the CysLT1R antagonist montelukast. The non-selective agonist LTD4 at 0.1 to 10 nM also induced a mild migration; however, the selective agonist N-methyl-LTC4 and the selective antagonist Bay cysLT2 for CysLT2R had no effects. Moreover, CysLT1R siRNA inhibited TGF-ß 1- and LTD4-induced astrocyte migration by down-regulating the expression of this receptor. However, TGF-ß 1 and LTD4 at various concentrations did not affect astrocyte proliferation 24 h after exposure. On the other hand, TGF-ß 1 increased 5-LOX expression and the production of CysLTs, and up-regulated CysLT1R (not CysLT2R), while LTD4 and N-methyl-LTC4 did not affect TGF-ß 1 expression and release. CONCLUSIONS: TGF-ß 1-induced astrocyte migration is, at least in part, mediated by enhanced endogenous CysLTs through activating CysLT1R. These findings indicate that the interaction between the cytokine TGF-ß 1 and the pro-inflammatory mediators CysLTs in the regulation of astrocyte function is relevant to glial scar formation.

[Effect of montelukast on morphological changes in neurons after ischemic injury].

OBJECTIVE: To determine the effect of montelukast, a cysteinyl leukotriene receptor 1 antagonist, on morphological changes in rat neurons after ischemic injury. METHODS: The in vivo ischemia injury was induced by oxygen-glucose deprivation (OGD) for 2 h and reperfusion (R) for 24 h (OGD/R) in rat neurons primary culture and mixed cortex culture. In the presence or absence of various concentrations of montelukast, neuron number, area of neuron, number of neuritis per neuron, branch number of primary neuritis and primary neurite length were determined for evaluating morphological changes in neurons. RESULTS: OGD/R significantly reduced neuron number, and altered neuron morphology. In cortical neuron cultures, montelukast (0.0001-1 µmol/L) attenuated OGD/R-induced reduction in neuron number, and inhibited OGD/R-induced increase in branch number of primary neuritis. In the mixed cultures, montelukast (0.0001-0.1 µmol/L) increased the primary neurite length, and reduced number of neuritis and branch number of primary neurite after OGD/R. CONCLUSION: Montelukast has a protective effect on ischemic injury in neurons.

[Cysteinyl leukotriene receptor 1 is involved in rotenone-induced injury of PC12 cells].

OBJECTIVE: To investigate whether cysteinyl leukotriene receptor 1 (CysLT1 receptor) is involved in rotenone-induced injury of PC12 cells. METHODS: After 24 h treatment with rotenone or with rotenone and the CysLT1 receptor antagonist montelukast, PC12 cell viability was determined by the colorimetric MTT reduction assay. After PC12 cells were treated with various concentrations of rotenone for 24 h or with 3 µmol/L rotenone for various durations, the expression of CysLT(1) receptor was determined by Western blotting, and its intracellular distribution was detected by immunocytochemistry. RESULTS: Rotenone (0.3-30 µmol/L) induced PC12 cell injury; this injury was significantly attenuated by montelukast at 1 and 5 µmol/L.The expression of CysLT(1) receptor increased after rotenone treatment at 1-10 µmol/L, or at 3 µmol/L for 3 and 24 h. Rotenone caused concentration-and time-dependent translocation of CysLT1 receptor from the nucleus to the cytosol. CONCLUSION: Cysteinyl leukotriene receptor 1 is involved in rotenone-induced injury of PC12 cells.

[Effects of agonist and antagonist of cysteinyl leukotriene receptors on differentiation of rat glioma C6 cells].

OBJECTIVE: To investigate the role of cysteinyl leukotriene (CysLT) receptors in the differentiation of rat glioma C6 cells. METHODS: Rat glioma C6 cells were treated with the agonist LTD(4), the CysLT(1) receptor antagonist montelukast and the differentiation inducer forskolin. Cell morphology and GFAP protein expression were determined after treatments. RESULT: Forskolin (10 µmol/L) induced morphological changes and GFAP protein expression (cell differentiation) in C6 cells, but LTD(4) (0.1-100 nmol/L) did not induce these changes. Montelukast (1 µmol/L) alone did not affect C6 cell differentiation, while it induced the differentiation when combined with the LTD(4) (100 nmol/L). CONCLUSION: The CysLT(2) receptor may modulate the differentiation of rat glioma C6 cells.

CysLT2 receptor-mediated AQP4 up-regulation is involved in ischemic-like injury through activation of ERK and p38 MAPK in rat astrocytes.

AIMS: We previously reported that cysteinyl leukotriene receptor 2 (CysLT(2)) mediates ischemic astrocyte injury, and leukotriene D(4)-activated CysLT(2) receptor up-regulates the water channel aquaporin 4 (AQP4). Here we investigated the mechanism underlying CysLT(2) receptor-mediated ischemic astrocyte injury induced by 4-h oxygen-glucose deprivation and 24-h recovery (OGD/R). MAIN METHODS: Primary cultures of rat astrocytes were treated by OGD/R to construct the cell injury model. AQP4 expression was inhibited by small interfering RNA (siRNA). The expressions of AQP4 and CysLTs receptors, and the MAPK signaling pathway were determined. KEY FINDINGS: OGD/R induced astrocyte injury, and increased expression of the CysLT(2) (but not CysLT(1)) receptor and AQP4. OGD/R-induced cell injury and AQP4 up-regulation were inhibited by a CysLT(2) receptor antagonist (Bay cysLT2) and a non-selective CysLT receptor antagonist (Bay u9773), but not by a CysLT(1) receptor antagonist (montelukast). Knockdown of AQP4 by siRNA attenuated OGD/R injury. Furthermore, OGD/R increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the cell injury and AQP4 up-regulation. SIGNIFICANCE: The CysLT(2) receptor mediates AQP4 up-regulation in astrocytes, and up-regulated AQP4 leads to OGD/R-induced injury, which results from activation of the ERK1/2 and p38 MAPK pathways.

[Studies on characteristics of volatile oil and micro-identification between Herba Pogostemonis and Herba Agastachis rugosae].

OBJECTIVE: To compare the chemical components of Herba Pogostemonis and Herba Agastachis rugosae, and develop a new method for the identification of them. METHODS: Comparing the chemical components in volatile oil of Herba Pogostemonis and Herha Agastachis rugosae by GC-MS, and identifying leaves of them by micro-characteristics. RESULTS: Patchouli alcohol (71.45%), the major component of Herba Pogostemonis, was its characteristic constituent and pulegone (37.58%) was the major component and characteristic constituent of Herba Agastachis rugosae. Two cells formed the head of glandular hairy in Herba Pogostemonis, while only one formed the head of glandular hairy in Herba Agastachis rugosae. The nonglandular hair was mainly constituted by one to three cells in Herba Pogostemonis, while one to four cells constituted the nonglandular hair in Herba Agastachis rugosae. CONCLUSION: A simple and dependable identification method has been developed for Herba Pogostemonis and Herba Agastachis rugosae.